RESUMO
ABSTRACT Objective: circCPA4 has been defined to be an oncogenic gene. This study examined whether circCPA4 regulates Prostate Cancer (PC) development and revealed its molecular mechanism. Methods: PC tissues and PC cell lines were collected, in which circCPA4/miR-491-5p/SHOC2 levels were evaluated by RT-qPCR and immunoblot. Colony formation assay and EdU assay assessed cell proliferation, flow cytometry measured apoptosis, and Transwell assessed invasion and migration. Ki-67, cleaved caspase-3, E-cadherin, and N-cadherin were evaluated by immunoblot. Based on the luciferase reporter assay and RIP assay the authors investigated the targeting relationship between circCPA4/miR-491-5p/SHOC2. The effect of circCPA4 on tumor growth was evaluated by xenotransplantation in nude mice. Results: circCPA4 and SHOC2 levels were abundant while miR-491-5p expression was low in PC. Loss of circCPA4 decreased the proliferation and EdU-positive rate of PC cells, enhanced apoptosis, and inhibited invasion, migration, and EMT. Upregulation of circCPA4 forced the malignant behaviors of PC cells, and this promotion could be abolished when miR-491-5p was overexpressed or SHOC2 was silenced. CircCAP4 competitively decoyed miR-491-5p mediating SHOC2 expression. circCAP4 suppression inhibited PC tumor growth. Conclusion: circCAP4 acts as a novel oncogenic factor in PC, accelerating the malignant behavior of PC cells via miR-491-5p/SHOC2 interaction. This novel ceRNA axis may be a potential target for PC drug development and targeted therapy in the future.
RESUMO
Aim To investigate the role and potential mechanism of methyltransferase-like 5 (METTL5) in triple-negative breast cancer (TNBC) . Methods The expression of METTL5 in TNBC tumor tissues and cell lines was detected by immunohistochemistry and Western blot. After shRNA targeting METTL5 (shRNAMETTL5) was transfected into TNBC cells, cell proliferation, migration and invasion were detected by CCK-8, colony formation, wound healing and Transwell assays, respectively. Western blot was used to detect the expression of Wnt/p-catenin signaling-related key proteins. A xenograft tumor model was constructed to verify the effect of METTL5 knockdown on the growth of TNBC cells and Wnt/p-catenin signaling activity in vivo. Results The expression of METTL5 was up-regulated in TNBC tumor tissues and cell lines (P < 0. 01) . Knockdown of METTL5 significantly inhibited the proliferation, migration and invasion of TNBC cells and reduced the expression of Wnt/p-catenin signaling molecules (3-catenin, cyclin Dl, matrix metalloproteinase (MMP) -2 and MMP-7 (all P < 0. 01) . Knockdown of METTL5 reduced tumor growth and Wnt/pcatenin signaling activity in vivo. Conclusions Knockdown of METTL5 can inhibit the proliferation, migration and invasion of TNBC cells, which may be related to the inhibition of Wnt/p-catenin signaling pathway.
RESUMO
OBJECTIVE To investigate the effects of polydatin （PD） on cell proliferation， migration， invasion and tumor growth of acute myeloid leukemia （AML）. METHODS Human AML cell KG-1 were divided into normal group， PD low-， medium- and high-concentration groups （10， 30， 60 μmol/L PD）， SQ22536 group [cyclic adenosine monophosphate （cAMP） inhibitor， 100 μmol/L]， high concentration of PD+SQ22536 group （60 μmol/L PD+100 μmol/L SQ22536）. The effects of PD on cell activity， apoptotic rate， invasion and migration ability， cAMP level， the expression of epithelial-mesenchymal transition （EMT） related proteins and protein kinase A （PKA） were investigated. Using BALB/c nude mice as subjects， a transplanted tumor model of AML nude mice was induced by subcutaneous inoculation of KG-1 cell suspension and then divided into control group， PD group， SQ22536 group and PD+SQ22536 group （with 6 mice in each group）. The effects of PD on tumor volume and mass were measured. RESULTS Compared with the normal group or control group， the cell viabilities， the number of migrating cells， the number of invasive cells， the relative expressions of vimentin and Snail as well as the tumor volume and mass were decreased significantly in PD groups， while the apoptotic rates， cAMP levels， the relative expressions of E-cadherin and PKA were significantly increased， with a dose-dependent manner （P＜0.05）. SQ22536 had opposite effects on cells and nude mice compared to PD， and could significantly reverse the anti-tumor activity of PD （P＜0.05）. CONCLUSIONS PD may inhibit the proliferation， migration， invasion and EMT process of KG-1 cells， induce apoptosis， and inhibit tumor growth， by activating the cAMP/PKA signaling pathway， thereby exerting anti-AML effects.
RESUMO
OBJECTIVE To investigate the effect and mechanism of picroside Ⅱ on the malignant progression of non-small cell lung cancer （NSCLC）. METHODS A549 cells were divided into the control group， picroside Ⅱ low-， medium- and high- concentration groups， K6PC-5 [sphingosine kinase 1 （SPHK1） activator] group， and picroside Ⅱ high-dose+K6PC-5 group. Cell proliferation， migration and invasion were detected. Besides， the expression of proliferating cell nuclear antigen （PCNA）， matrix metalloproteinase-2 （MMP-2）， MMP-9， SPHK1， sphingosine-1-phosphate receptor 3 （S1PR3） and extracellular signal-regulated kinase 1/2 （ERK1/2） protein in the cells were also observed. BALB/c nude mice were subcutaneously inoculated with A549 cell suspension to establish NSCLC xenograft models. Then they were assigned to the nude mouse-control group， nude mouse-picroside Ⅱ low-， medium- and high-dose groups， nude mouse-K6PC-5 group， and nude mouse-picroside Ⅱ high-dose+K6PC-5 group （with 5 mice in each group） to investigate the effect of picroside Ⅱ on their tumor mass and volume. RESULTS Compared with the control group， the OD450 values， EdU-positive cell rates， scratch healing rates， cell invasion number， and the relative expression levels of PCNA， MMP-2， MMP-9， SPHK1， S1PR3 and ERK1/2 protein in the low-， medium- and high-concentration groups of picroside Ⅱ were significantly decreased. Compared with the nude mouse-control group， the tumor mass and volume in the nude mouse-low-， medium- and high-dose groups of picroside Ⅱ were significantly decreased or shrunk. The changes of above indicators were concentration/dose-dependent （P＜0.05）. The changing trend of the corresponding indicators in the K6PC-5 ZYTS181） group and the nude mouse-K6PC-5 group was opposite （P＜0.05）. Compared with the picroside Ⅱ high-concentration group or the nude mice-picroside Ⅱ high-dose group， the above quantitative indicators in the picroside Ⅱ high- concentration+K6PC-5 group cells and the nude mouse-picroside Ⅱ high-dose+K6PC-5 group nude mice were significantly increased or enlarged （P＜0.05）. CONCLUSIONS Picroside Ⅱ may inhibit the malignant progression of NSCLC by inhibiting SPHK1/sphingosine-1-phosphate/S1PR3 signaling pathway.
RESUMO
ObjectiveTo investigate the expression level of Golgi transport 1A （GOLT1A） in thyroid carcinoma and its effects on the proliferation， migration， invasion， and epithelial-mesenchymal transition （EMT） of thyroid carcinoma cells. MethodsThe expression of GOLT1A in thyroid carcinoma was analyzed online by tumor immune estimation resource （TIMER）， the University of Alabama at Birmingham cancer data analysis portal （UALCAN）， gene expression profiling interactive analysis 2 （GEPIA2）. The expression level of GOLT1A in thyroid carcinoma cells was detected by real-time fluorescence quantitative polymerase chain reaction （RTFQ-PCR） and western blot. Cell counting kit-8 （CCK-8） assay， colony formation assay， and transwell assay were used to detect the effects of GOLT1A expression on the proliferation， migration， and invasion of thyroid carcinoma cells. Western blot assay was used to detect the effect of GOLT1A on the expression of EMT-related genes including E-cadherin， vimentin， and N-cadherin. ResultsThe online analysis of GEPIA2， TIMER， and UALCAN showed that the expression of GOLT1A was higher in thyroid carcinoma than in normal tissues， and the expression of GOLT1A in thyroid carcinoma cells was significantly higher than in normal control cells. Knockdown of GOLT1A inhibited TPC1 cell proliferation， migration， and invasion. The expression of E-cadherin increased and the expressions of N-cadherin and vimentin decreased in GOLT1A knockdown TPC1 cells. Overexpression of GOLT1A promoted BCPAP cell proliferation， migration， and invasion. The expression of E-cadherin decreased and the expressions of N-cadherin and vimentin increased in GOLT1A overexpression BCPAP cells. ConclusionGOLT1A is highly expressed in thyroid carcinoma and can promote the proliferation， migration， and invasion of thyroid carcinoma cells.
RESUMO
Background: Tumor size is an independent predictor of lymph node metastasis and survival in the endometrioid type endometrial adenocarcinoma (EC). However, some of the ECs tend to grow towards the cavity in the polypoid pattern, which can reach very large sizes. In this study, we aimed to analyze the association of growing in the polypoid pattern of the tumor with the proportion of lymph node metastasis and extrauterine tumor spread. Methods: Four hundred seven patients were analyzed retrospectively. The effect of tumor size, tumor growing pattern, myometrial invasion, grade, and lymphovascular space invasion on the lymph node metastasis and extrauterine tumor spread were investigated. Statistical analysis consisted of unpaired t?tests for parametric data and Mann Whitney?U test for non?parametric data, whereas the Chi?square test for categorical variables. Logistic Regression, Cox Regression and multivariate analysis were used to estimate the risk predictors. Results: No association was found between the growing in polypoid pattern and lymph node metastasis (P > 0.05). In the analysis of endometrioid type EC patients who had myometrial invasion less than � as a subgroup, no association was found between the growing pattern and lymph node metastasis and extrauterine disease. Tumor size was found to be a statistically significant predictor of lymph node metastasis and extrauterine disease (P < 0.05). Conclusions: Lymphovascular space invasion, grade, and myometrial invasion are associated with a higher proportion of lymph node metastasis. The polypoid growth pattern of the tumor does not correlate with any histopathological parameters
RESUMO
Abstract Objective This study aimed to investigate the molecular mechanism of miR-150-5p regulating the malignant biological behavior of Human Epidermoid cancer cell (HEp-2) by targeting peptidyl-prolyl cis/trans isomerase NIMA-Interacting-1 (PIN1). Methods Firstly, qRT-PCR and Western blot were adopted to detect the expression levels of miR-150-5p and PIN1 in cancer tissue and paracancerous tissues of patients with LSCC, and those in human bronchial epithelial cells (16 HBE) and HEp-2. Next, the targeted relationship between miR-150-5p and PIN1 was assessed by bioinformatics website and dual-luciferase reporter assay, followed by their correlation analysis. Besides, after interfering with miR-150-5p or PIN1 expression in HEp-2 cells, CCK-8, cell colony formation assay, and transwell assay were utilized to detect the proliferation, viability, and invasion of cells, respectively. Subsequently, the protein levels of MMP-2, MMP-9, and EMT-related proteins in HEp-2 cells were checked by Western blot. Results Expression of miR-150-5p was down-regulated in LSCC tissues and HEp-2 cells. Moreover, miR-150-5p suppressed proliferation and invasion of HEp-2 cells, affected protein expression related to MMP and EMT, thereby inhibiting development of cancer. The expression of PIN1 was significantly increased in cancer tissues and HEp-2 cells, and there was a targeted relationship and negative correlation between miR-150-5p and PIN1 in cancer tissue. However, overexpression of PIN1 could reverse the effect of miR-150-5p on the proliferation and invasion of HEp-2 cells. Conclusion In a nutshell, there is a targeted relationship between PIN1 and miR-150-5p. Besides, miR-150-5p can inhibit the proliferation and invasion of HEp-2 cells by regulating the expression of PIN1. Level of evidence 3.
RESUMO
Inadequate invasion and excessive apoptosis of trophoblast cells are associated with the development of preeclampsia. Vitamin D deficiency in pregnant women may lead to an increased risk of preeclampsia. However, the underlying mechanisms by which vitamin D is effective in preventing preeclampsia are not fully understood. The objectives of this study were to investigate the role of lysosome-associated membrane glycoprotein 3 (LAMP3) in the pathogenesis of preeclampsia and to evaluate whether vitamin D supplementation would protect against the development of preeclampsia by regulating LAMP3 expression. Firstly, the mRNA and protein levels of LAMP3 were significantly upregulated in the placentas of preeclampsia patients compared to normal placentas, especially in trophoblast cells (a key component of the human placenta). In the hypoxia/reoxygenation (H/R)-exposed HTR-8/Svneo trophoblast cells, LAMP3 expression was also upregulated. H/R exposure repressed cell viability and invasion and increased apoptosis of trophoblast cells. siRNA-mediated knockdown of LAMP3 increased cell viability and invasion and suppressed apoptosis of H/R-exposed trophoblast cells. We further found that 1,25(OH)2D3 (the hormonally active form of vitamin D) treatment reduced LAMP3 expression in H/R exposed trophoblast cells. In addition, 1,25(OH)2D3 treatment promoted cell viability and invasion and inhibited apoptosis of H/R-exposed trophoblast cells. Notably, overexpression of LAMP3 abrogated the protective effect of 1,25(OH)2D3 on H/R-exposed trophoblast cells. Collectively, we demonstrated trophoblast cytoprotection by vitamin D, a process mediated via LAMP3.
RESUMO
Resumen ANTECEDENTES: La vasculatura miometrial aumentada es una afección poco común, con alto riesgo de hemorragia masiva. Su fisiopatología se relaciona con una remodelación inadecuada del endometrio y miometrio, posterior a un evento obstétrico. El tratamiento convencional, en caso de sangrado masivo, es la histerectomía. En la actualidad, los tratamientos con enfoque conservador que permiten el embarazo espontáneo, ofrecen una opción segura para estas pacientes. CASO CLÍNICO: Paciente de 20 años, primigesta, con deseo gestacional a futuro, llevada a la sala de urgencias debido a una hemorragia uterina profusa, con datos clínicos de bajo gasto, antecedente de aborto completo de 10 semanas de gestación un mes antes. En el ultrasonido Doppler se observó una imagen anecoica irregular en el fondo uterino que interrumpía la interfase endometrio-miometrial asociada con flujo sistólico alto. Para el control vascular se indicó cirugía conservadora de útero, con ligadura temporal laparoscópica de las arterias uterinas; además aspiración uterina. Estos procedimientos trascurrieron sin complicaciones. El reporte histopatológico del material aspirado fue de tejido trofoblástico asociado con ectasia vascular. CONCLUSIÓN: La ligadura temporal laparoscópica de las arterias uterinas es un procedimiento eficaz, en casos seleccionados, de control vascular durante la extracción del tejido trofoblástico remanente, en casos de vasculatura miometrial aumentada, relacionada con el embarazo, con recuperación completa de la irrigación uterina y preservación del útero.
Abstract BACKGROUND: Enlarged myometrial vasculature is a rare condition with a high risk of massive haemorrhage. Its pathophysiology is related to inadequate remodelling of the endometrium and myometrium following an obstetric event. The conventional treatment for massive haemorrhage is hysterectomy. Currently, conservative management approaches that allow spontaneous pregnancy offer a safe option for these patients. CLINICAL CASE: 20-year-old primigravida with future pregnancy aspirations, presented to the emergency department with heavy uterine bleeding, clinical data of low output, history of complete abortion at 10 weeks' gestation one month earlier. Doppler ultrasound showed an irregular anechoic image in the uterine fundus interrupting the endometrial-myometrial interface associated with high systolic flow. For vascular control, uterine-sparing surgery with laparoscopic temporary ligation of the uterine arteries and uterine aspiration was indicated. These procedures were performed without complications. The histopathological report of the aspirated tissue was trophoblastic tissue associated with vascular ectasia. CONCLUSION: Temporary laparoscopic ligation of the uterine arteries is an effective procedure in selected cases for vascular control during removal of the remaining trophoblastic tissue, in cases of pregnancy-related increased myometrial vasculature, with complete recovery of uterine irrigation and preservation of the uterus.
RESUMO
La tetralogía de Fallot es la cardiopatía congénita cianótica más frecuente, su prevalencia es del 0,08% afectando aproximadamente a 1 de cada 8.500 nacidos vivos. El manejo de pacientes con cardiopatía congénita representa un desafío para el odontopediatra, ya que requiere conocimientos y habilidades específicas. La odontología de mínima intervención permite ofrecer a los pacientes un tratamiento gentil, mejorando el abordaje conductual ayudando a la adaptación del paciente al tratamiento dental. El objetivo de este reporte consiste describir el manejo estomatológico con odontología de mínima intervención en una paciente femenina de 5 años de edad con diagnóstico de tetralogía de Fallot. Conclusión: la odontología de mínima intervención fue eficaz para el tratamiento de paciente con cardiopatía congénita aportando herramientas significativas destinadas a mejorar la conducta, brindando tratamientos sencillos, rápidos y conservadores. Dando la posibilidad de este tipo de tratamientos en cualquier otro paciente con compromiso médico
A tetralogia de Fallot é a cardiopatia congênita cianótica mais comum, com uma prevalência de 0,08%, afetando aproximadamente 1 em 8.500 nascidos vivos. O tratamento de pacientes com cardiopatias congênitas representa um desafio para os dentistas pediátricos, pois requer conhecimentos e habilidades específicas. A odontologia de intervenção mínima permite oferecer aos pacientes um tratamento gentio, melhorando a abordagem comportamental e ajudando na adaptação do paciente ao tratamento odontológico. O objetivo deste relatório é descrever o tratamento estomatológico com intervenção odontológica mínima em um paciente de 5 anos diagnosticado com tetralogia de Fallot. Conclusão: A odontologia com intervenção mínima foi eficaz no tratamento de pacientes com doenças cardíacas congênitas, fornecendo ferramentas significativas destinadas a melhorar o comportamento, oferecendo tratamentos simples, rápidos e conservadores. Ela oferece a possibilidade deste tipo de tratamento em qualquer outro paciente com comprometimento médico
Tetralogy of Fallot is the most common cyanotic congenital heart disease, with a prevalence of 0,08%, affecting approximately 1 in every 8,500 live births. Treatment patients with congenital heart disease represents a challenge for pediatric dentists, it requires specific knowledge and skills. Minimal intervention dentistry allows offering patients a gentle treatment, improving the behavioral approach and helping the patient's adaptation to dental treatment. The aim of this report is to describe the management with minimal intervention dentistry in a 5-year-old female patient with a diagnosis of tetralogy of Fallot. Conclusion: Minimal intervention dentistry was effective in the treatment of patients with congenital heart disease, providing significant tools aimed at improving behavior, offering simple, fast and conservative treatments. It gives the possibility of this type of treatment in any other patient with medical compromise.
Assuntos
Humanos , Pré-Escolar , CriançaRESUMO
Abstract Objectives: Lung cancer was one of the most common malignancies around the world. It has great significance in to search for the mechanism of occurrence and development of lung cancer. LIM Domain Binding protein 2 (LDB2) belongs to the LIM-domain binding family, it can be used as a binding protein that combined with other transcription factors to form the transcription complex for regulating the expression of target genes. The expression of microRNA-96-5p (miR-96-5p) has been investigated in various tumors. The aim of this study is to investigate the potential role of LDB2 and miR-96-5p in lung cancer. Methods: Real-time quantitative PCR was applied to detect the expression of LDB2 and miR-96-5p. The proliferation, invasion, and metastasis of H1299 cells were analyzed by CCK8, transwell, and wound healing assay after LDB2 or miR-96-5p transfection. Luciferase activities assay and western blot were used to reveal the targeted regulation between LDB2 and miR-96-5p. Results: Here the authors found LDB2 was down-regulated in lung cancer tissues and negatively correlated with miR-96-5p expression, it could promote or inhibit the proliferation, invasion and metastasis of H1299 cells after LDB2 knockdown or overexpression and regulate the expression of cyclinD1, MMP9, Bcl-2, and Bax via ERK1/2 signaling pathway. Furthermore, miR-96-5p exerted its function by directly binding to 3′-UTR of LDB2 and regulating expression of LDB2. miR-96-5p could promote the proliferation, invasion, and metastasis of H1299 cells. Conclusion: These findings demonstrate that LDB2 can act as a new regulator to inhibit cell proliferation, invasion, and metastasis via the ERK1/2 signaling pathway, and miR-96-5p may be a potential promising molecular by targeting LDB2 in lung cancer.
RESUMO
ABSTRACT Objectives: We examined the expression of Lnc-ZFAS1 in osteosarcoma and comprehensively evaluated its effects on osteosarcoma in vitro and vivo. Moreover, we revealed the regulatory mechanism between Lnc-ZFAS1 and miR-520b/miR-520e-mediated RHOC and provided a novel clue for ameliorating osteosarcoma. Method: The expression of Long non-coding RNA Zinc Finger Antisense 1 (LncRNA ZFAS1) osteosarcoma tissues and normal tissues in the TCGA database was analyzed. Then, LncRNA ZFAS1 expression was further verified in clinical samples and osteosarcoma cell lines (U2OS and KHOS), as well as the human osteoblast cell line hFOB1.19 by qRT-PCR. Thereafter, LncRNA ZFAS1 was overexpressed or silenced to explore its effects on cell proliferation, apoptosis, migration, invasion, and Epithelial-Mesenchymal Transition (EMT). The fundamental mechanism through which Lnc-ZFAS1 affects osteosarcoma progression was further investigated and verified. Results: We found that LncRNA ZFAS1 was upregulated in osteosarcoma, and Lnc-ZFAS1 overexpression facilitated osteosarcoma cells proliferation, migration, invasion and EMT, while Lnc-ZFAS1 silence exerted reverse influence. Mechanistically, Lnc-ZFAS1 functionally acted as a sponger of microRNA-520b (miR-520b) and micro-RNA-520e (miR-520e) to up-regulate Ras Homologue C (RHOC). In addition, depleted Lnc-ZFAS1 restrained osteosarcoma cells proliferation, migration, and invasion, which could be rescued by RHOC overexpression. Lnc-ZFAS1 was upregulated in osteosarcoma and Lnc-ZFAS1 could exert promoted impact upon osteosarcoma cells proliferation, migration, invasion, and EMT in vitro. Conclusions: Lnc-ZFAS1 acted sponger of miR-520b and miR-520e to promote RHOC, indicating that Lnc-ZFAS1/miR-520b/RHOC and Lnc-ZFAS1/miR-520e/RHOC axes might serve as potential therapeutic strategies against osteosarcoma.
RESUMO
Abstract Mytilopsis leucophaeata is an estuarine bivalve native from the Gulf of Mexico and Southeast USA, and it was introduced in Europe, Asia, Caribbean, South America and Northeast USA, showing massive colonization skills. In Brazil, the single invasion records of M. leucophaeata occur in the city of Rio de Janeiro, i.e., in the Rodrigo de Freitas Lagoon and in the Marapendi Lagoon. We conducted a new series of fieldworks in estuaries from the Rio de Janeiro state in order to evaluate the propagation of this invasive bivalve, aiming sites with proper salinities for the establishment of M. leucophaeata. A new record is given for the Maricá-Guarapina lagoon system, where M. leucophaeata mainly colonizes hard substrata (such as piers and rocks), reaching a mean density up to 43,375 specimens/m2; however, aggregates of M. leucophaeata were also observed in the soft substratum. Based on mitochondrial sequences, the taxonomic identification of the invasive bivalve was confirmed. The associated fauna to the agglomerates of M. leucophaeata in the lagoon system comprises amphipods, barnacles, tanaidaceans, isopods, crabs, polychaetes and snails. The expansion of M. leucophaeata requires a continuous investigation due to the great circulation of boats in the littoral of the Rio de Janeiro state and the increased chance of new introductions.
Resumo Mytilopsis leucophaeata é um bivalve estuarino originário do Golfo do México e Sudeste dos EUA, tendo sido introduzido na Europa, Ásia, Caribe, América do Sul e Nordeste dos EUA, e apresentando massiva capacidade de colonização. No Brasil, os únicos registros de invasão de M. leucophaeata ocorrem no município do Rio de Janeiro, i.e., na Lagoa Rodrigo de Freitas e na Lagoa de Marapendi. Este estudo propõe um novo levantamento de campo em estuários fluminenses para avaliar a propagação desse bivalve invasor, visando locais com salinidade propícia para o estabelecimento de M. leucophaeata. Um novo registro é feito para o complexo lagunar Maricá-Guarapina, onde M. leucophaeata coloniza principalmente substratos duros (como píers e rochas), chegando a uma densidade média de 43.375 indíviduos/m2; porém, agregados de M. leucophaeata também foram observados em substrato inconsolidado. Com base em sequências mitocondriais, a identificação taxonômica do bivalve invasor foi confirmada. A fauna associada aos aglomerados de M. leucophaeata no complexo lagunar compreende anfípodes, cracas, tanaidáceos, isópodes, caranguejos, poliquetas e gastrópodes. A expansão de M. leucophaeata demanda uma investigação contínua devido ao alto fluxo de embarcações no litoral fluminense e elevada probabilidade de novas introduções.
RESUMO
Abstract The power of computed tomography (CT) radiomics for preoperative prediction of microvascular invasion (MVI) in hepatocellular carcinoma (HCC) demonstrated in current research is variable. This systematic review and meta-analysis aim to evaluate the value of CT radiomics for MVI prediction in HCC, and to investigate the methodologic quality in the workflow of radiomics research. Databases of PubMed, Embase, Web of Science, and Cochrane Library were systematically searched. The methodologic quality of included studies was assessed. Validation data from studies with Transparent Reporting of a Multivariable Prediction Model for Individual Prognosis or Diagnosis (TRIPOD) statement type 2a or above were extracted for meta-analysis. Eleven studies were included, among which nine were eligible for meta-analysis. Radiomics quality scores of the enrolled eleven studies varied from 6 to 17, accounting for 16.7%-47.2% of the total points, with an average score of 14. Pooled sensitivity, specificity, and Area Under the summary receiver operator Characteristic Curve (AUC) were 0.82 (95% CI 0.77-0.86), 0.79 (95% CI 0.75-0.83), and 0.87 (95% CI 0.84-0.91) for the predictive performance of CT radiomics, respectively. Meta-regression and subgroup analyses showed radiomics model based on 3D tumor segmentation, and deep learning model achieved superior performances compared to 2D segmentation and non-deep learning model, respectively (AUC: 0.93 vs. 0.83, and 0.97 vs. 0.83, respectively). This study proves that CT radiomics could predict MVI in HCC. The heterogeneity of the included studies precludes a definition of the role of CT radiomics in predicting MVI, but methodology warrants uniformization in the radiology community regarding radiomics in HCC.
RESUMO
OBJECTIVE@#To investigate the effect of Porphyromonas gingivalis (Pg) infection on IFNGR1 palmitoylation and biological behaviors of esophageal squamous cell carcinoma (ESCC) cells and the clinical implications.@*METHODS@#The expression levels of IFNGR1 protein in ESCC cell lines KYSE30 and KYSE70 were detected using Western blotting at 24 and 48 h after Pg infection, and 2-BP was used to detect IFNGR1 palmitoylation in the cells. KYSE70 cells with wild-type IFNGR1 (IFNGR1-WT cells) and with IFNGR1-C122A palmitoylation site mutation induced by site-specific mutagenesis (IFNGR1-C122A cells) were both infected with Pg, and the changes in palmitoylation of IFNGR1-C122A were analyzed using immunofluorescence and Click-iT assays. The changes in proliferation, migration and invasion ability of the infected cells were evaluated using plate cloning assay, scratch assay and Transwell assay, and IFNGR1 co-localization with lysosomal marker LAMP2 was dected using immunofluorescence assay. Immunohistochemistry was used to detect Pg infection and IFNGR1 protein expression in 50 ESCC tissues, and their correlation with the clinicopathological characteristics and survival outcomes of the patients was analyzed.@*RESULTS@#Pg infection down-regulated the protein expression of IFNGR1 in ESCC and promoted IFNGR1 palmitoylation at site 122. In IFNGR1-WT cells, Pg infection significantly enhanced cell proliferation, migration and invasion (P < 0.05). Similarly, Pg also significantly promoted proliferation, migration and invasion of IFNGR1-C122A cells, but to a lesser extent as compared with the wild-type cells (P < 0.05). Immunofluorescence assay showed that Pg and ZDHHC3 promoted IFNGR1 degradation within the lysosome. Immunohistochemical studies of the ESCC tissue samples showed a negative correlation between IFNGR1 and Pg expression, and a reduced IFNGR1 expression was correlated with a poorer survival outcome of the patient.@*CONCLUSION@#Pg infection enhances IFNGR1 palmitoylation to promote progression of ESCC, and elimination of Pg and inhibiting IFNGR1 palmitoylation may effectively control ESCC progression.
Assuntos
Humanos , Neoplasias Esofágicas , Porphyromonas gingivalis , Lipoilação , Carcinoma de Células Escamosas do Esôfago , LisossomosRESUMO
OBJECTIVE@#To investigate the consistency and diagnostic performance of magnetic resonance imaging (MRI) for detecting microvascular invasion (MVI) of hepatocellular carcinoma (HCC) and the validity of deep learning attention mechanisms and clinical features for MVI grade prediction.@*METHODS@#This retrospective study was conducted among 158 patients with HCC treated in Shunde Hospital Affiliated to Southern Medical University between January, 2017 and February, 2020. The imaging data and clinical data of the patients were collected to establish single sequence deep learning models and fusion models based on the EfficientNetB0 and attention modules. The imaging data included conventional MRI sequences (T1WI, T2WI, and DWI), enhanced MRI sequences (AP, PP, EP, and HBP) and synthesized MRI sequences (T1mapping-pre and T1mapping-20 min), and the high-risk areas of MVI were visualized using deep learning visualization techniques.@*RESULTS@#The fusion model based on T1mapping-20min sequence and clinical features outperformed other fusion models with an accuracy of 0.8376, a sensitivity of 0.8378, a specificity of 0.8702, and an AUC of 0.8501 for detecting MVI. The deep fusion models were also capable of displaying the high-risk areas of MVI.@*CONCLUSION@#The fusion models based on multiple MRI sequences can effectively detect MVI in patients with HCC, demonstrating the validity of deep learning algorithm that combines attention mechanism and clinical features for MVI grade prediction.
Assuntos
Humanos , Carcinoma Hepatocelular , Estudos Retrospectivos , Neoplasias Hepáticas , Imageamento por Ressonância Magnética , AlgoritmosRESUMO
OBJECTIVE@#To investigate the effects of expression levels of S100 calcium-binding protein A10 (S100A10) in lung adenocarcinoma (LUAD) on patient prognosis and the regulatory role of S100A10 in lung cancer cell proliferation and metastasis.@*METHODS@#Immunohistochemistry was used to detect the expression levels of S100A10 in LUAD and adjacent tissues, and the relationship between S100A10 expression and clinicopathological parameters and prognosis of the patients was statistically analyzed. The lung adenocarcinoma expression dataset in TCGA database was analyzed using gene enrichment analysis (GSEA) to predict the possible regulatory pathways of S100A10 in the development of lung adenocarcinoma. Lactate production and glucose consumption of lung cancer cells with S100A10 knockdown or overexpression were analyzed to assess the level of glycolysis. Western blotting, CCK-8 assay, EdU-594 assay, and Transwell assays were performed to determine the expression level of S100A10 protein, proliferation and invasion ability of lung cancer cells. A549 cells with S100A10 knockdown and H1299 cells with S100A10 overexpression were injected subcutaneously in nude mice, and tumor growth was observed.@*RESULTS@#The expression level of S100A10 was significantly upregulated in LUAD tissues as compared with the adjacent tissues, and an elevated S100A10 expression level was associated with lymph node metastasis, advanced tumor stage and distant organ metastasis (P < 0.05), but not with tumor differentiation or the patients' age or gender (P > 0.05). Survival analysis showed that elevated S100A10 expressions in the tumor tissue was associated with a poor outcome of the patients (P < 0.001). In the lung cancer cells, S100A10 overexpression significantly promoted cell proliferation and invasion in vitro (P < 0.001). GSEA showed that the gene sets of glucose metabolism, glycolysis and mTOR signaling pathway were significantly enriched in high expressions of S100A10. In the tumor-bearing nude mice, S100A10 overexpression significantly promoted tumor growth, while S100A10 knockdown obviously suppressed tumor cell proliferation (P < 0.001).@*CONCLUSION@#S100A10 overexpression promotes glycolysis by activating the Akt-mTOR signaling pathway to promote proliferation and invasion of lung adenocarcinoma cells.
Assuntos
Animais , Camundongos , Humanos , Adenocarcinoma de Pulmão/patologia , Proliferação de Células , Neoplasias Pulmonares/patologia , Camundongos Nus , Proteínas Proto-Oncogênicas c-akt , Transdução de Sinais , Serina-Treonina Quinases TOR , Proteínas S100/genéticaRESUMO
The most common type of intracranial malignancy is glioma. Although the current treatments are surgery, radiation and chemotherapy, the prognosis for patients with glioma is not promising. Therefore, it becomes critical to find an effective management. The literature shows that microRNA (miRNA) plays an important role in tumorigenesis and progression. Based on this, this study aimed to investigate the molecular mechanism of miR-525-5p in regulating the migration, invasion and proliferation of glioma cells. The TCGA database was used to identify perilipin 3 (PLIN3) differentially expressed in normal tissues and glioma tissues, and the CGGA and GEPIA databases were used to query that high expression of PLIN3 was associated with poor prognosis in glioma patients and Western blot experiments revealed that PLIN3 was highly expressed in glioma cells (P<0. 05) . The results of wound healing assay and Transwell invasion assay showed that knockdown or overexpression of PLIN3 respectively inhibited or promoted the migration and invasion of glioma cells (P < 0. 05) . Dual luciferase assays confirmed that PLIN3 could bind to miR-525-5p target. Real-time fluorescence quantitative polymerase chain reaction (qRT-PCR) showed that miR-525-5p expression was lower in LN229 and U251 glioma cells than in human astrocyte (HA) (P < 0. 05) . Transwell assay and 5-ethynyl-2-deoxyuridine (EdU) cell proliferation assay verified that down- or up-regulation of miR-525-5p could reverse the effects of overexpression or knockdown of PLIN3 on LN229 glioma cells (P<0. 05) . Taken together, miR-525-5p was able to regulate the migration, invasion and proliferation of glioma cells by targeting PLIN3.
RESUMO
AIM: To explore the molecular mechanism of sequoiaflavone affecting gastric cancer cells. MEHTODS: Gastric cancer cell line AGS cells were treated with gradient concentrations of sequoiaflavone, and then induced by PI3K/AKT signaling pathway activator. The optimal inhibitory concentration and time of semi-inhibitory concentration of red cedar flavonoid on AGS cells were detected by CCK-8, and the changes of cell proliferation, migration and invasion ability were detected by colony formation assay, transwell assay and wound healing assay. PI3K/AKT signal pathway related proteins p-PI3K, PI3K, p-AKT and AKT were detected by western blot. RESULTS: Sequoiaflavone inhibited AGS cells in a concentration-dependent manner. The half inhibitory concentration was 0.5 mmol/L, the optimal treatment time was 48 h. The protein expression of p-PI3K and p-AKT was down regulated. The proliferation, migration and invasion of AGS cells were decreased after treated with sequoiaflavone. After treated with PI3K / AKT signal pathway activator, the protein expression level of pPI3K and p-AKT was partially reversed, and the ability of cell viability, proliferation, migration and invasion was also partially improved. CONCLUSION: Inactivation of PI3K/AKT signaling pathway caused by sequoiaflavone inhibited gastric cancer cells proliferation, migration and invasion ability.
RESUMO
Aim To observe the effect of betulinic acid (BA) on the migration and invasion of human gastric cancer MKN-45 cells induced by transforming growth factor-pi (TGF-β1), and to explore the effect of BA on epithelial-mesenchymal transition (EMT) and the potential mechanism. Methods The MKN-45 cells were cultivated in vitro, and the effects of different concentrations of BA on the proliferation of MKN-45 cells at 24, 48 and 72 h were detected using CCK-8 method. The effects of BA (5, 10, 20 jjunol • L) and TGF-01 inhibitor LY2109761 (10