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1.
Rev. cuba. invest. bioméd ; 40(2): e1189, 2021. tab, graf
Article in Spanish | LILACS, CUMED | ID: biblio-1347466

ABSTRACT

Introducción: El cáncer pulmonar constituye un serio problema de salud mundial por su elevada prevalencia y mortalidad. En la carcinogénesis pulmonar están implicados oncogenes y genes supresores tumorales, que en una compleja interacción con factores ambientales favorecen la transformación cancerosa. Objetivo: Describir los principales genes implicados en el cáncer pulmonar. Métodos: Se buscaron referencias en las bases de datos PubMed Central, Annual Reviews y SciELO. Se revisaron preferentemente los artículos originales, las revisiones bibliográficas, las revisiones sistemáticas y los metaanálisis de los últimos cinco años. Análisis e integración de la información: En la carcinogénesis pulmonar se involucran los oncogenes JUN, FOS, ABL1, BRAF, RAF1, GNAS, KRAS, NRAS, HRAS, CSF 1R, MYC, EGFR, MET, ALK, CCNE1, DDR2, ERBB3, FGFR1, MDM2, ROS1, SOX2 y TP63 y los genes supresores tumorales TP53, CDKN2A, CDKN1A, RB1, CDK2AP1, ATM, ERCC2, BRCA1, CCND1, STK11, PDLIM2, PTEN, ARID1A, ASCL4, CUL3, EP300, KEAP1, KMT2D, NF1, NOTCH1, RASA1, ETD2 y SMARCA4. El conocimiento de la genética molecular del cáncer pulmonar es importante para la identificación de biomarcadores diagnósticos y pronósticos más eficaces y para el diseño de fármacos diana sobre genes específicos(AU)


Introduction: Lung cancer is a serious global health problem due to its high prevalence and mortality. Lung carcinogenesis involves oncogenes and tumor suppressor genes which interact in complex manners with environmental factors, paving the way for the cancerous transformation. Objective: Describe the main genes involved in lung cancer. Methods: References were searched for in the databases PubMed Central, Annual Reviews and SciELO. Particular attention was paid to original papers, bibliographic reviews, systematic reviews and meta-analyses published in the last five years. Data analysis and integration: Lung carcinogenesis involves the oncogenes JUN, FOS, ABL1, BRAF, RAF1, GNAS, KRAS, NRAS, HRAS, CSF 1R, MYC, EGFR, MET, ALK, CCNE1, DDR2, ERBB3, FGFR1, MDM2, ROS1, SOX2 and TP63, and the tumor suppressor genes TP53, CDKN2A, CDKN1A, RB1, CDK2AP1, ATM, ERCC2, BRCA1, CCND1, STK11, PDLIM2, PTEN, ARID1A, ASCL4, CUL3, EP300, KEAP1, KMT2D, NF1, NOTCH1, RASA1, ETD2 and SMARCA4. Knowledge about the molecular genetics of lung cancer is important to identify more efficient diagnostic and prognostic biomarkers and to design targeted drugs for specific genes(AU)


Subject(s)
Humans , Oncogenes , Biomarkers , Genes, Tumor Suppressor
2.
Article in Chinese | WPRIM | ID: wpr-879266

ABSTRACT

In recent years, with the improvement of the sensitivity of examination equipment and the change of people's living environment and diet, the rate of thyroid cancer has risen rapidly, which has increased nearly five folds in 10 years. The pathogenesis, clinical manifestation, biological behavior, treatment and prognosis of thyroid carcinoma of different pathological types are obviously different. Papillary thyroid carcinoma (PTC) can develop at any age, which accounts for about 90% of thyroid cancer. It progresses slowly and has favourable prognosis, but lymph node metastasis appears easily. Whether PTC is accompanied by lymph node metastasis has an important impact on its prognosis and outcome. The Raf murine sarcoma viral oncogene homolog B(BRAF)gene mutation plays a crucial role in PTC lymph node metastasis. Having an in-depth understanding of the specific role and mechanism of BRAF gene mutation in PTC is expected to provide new ideas for diagnosis and treatment of PTC.


Subject(s)
Animals , Carcinoma, Papillary/genetics , Humans , Lymphatic Metastasis , Mice , Mutation , Oncogenes , Proto-Oncogene Proteins B-raf/genetics , Thyroid Cancer, Papillary/genetics , Thyroid Neoplasms/genetics
3.
Article in English | WPRIM | ID: wpr-922585

ABSTRACT

OBJECTIVES@#The biomarkers targeting colorectal cancer (CRC) prognosis are short of high accuracy and sensitivity in clinic. Through bioinformatics analysis, we aim to identify and confirm a series of key genes referred to the diagnosis and prognosis of CRC.@*METHODS@#GSE31905, GSE35279, and GSE41657 were selected as complete RNA sequencing data sets of CRC and colorectal mucosa (CRM) tissues from the NCBI-GEO database, and the differentially expressed genes (DEGs) were analyzed. The common DEGs in these 3 data sets were obtained by Venn map, and enriched by STRING network system and Cytoscape software. The Kaplan-Meier plotter website was used to verify the correlation between the enriched genes and the prognosis of CRC.@*RESULTS@#For the whole RNA sequencing data sets of CRC and normal intestinal mucosa samples, the DEGs of CRC and CRM in the 3 data sets (|log@*CONCLUSIONS@#The above 11 genes verified by bioinformatics retrieval and analysis can predict the poor prognosis of CRC to a certain extent, and they provide a possible target for the diagnosis and treatment of CRC.


Subject(s)
Biomarkers, Tumor/metabolism , Colorectal Neoplasms/genetics , Computational Biology , Formins , Gene Expression Profiling , Gene Expression Regulation, Neoplastic , Glycoproteins , Humans , Intercellular Signaling Peptides and Proteins , Oncogenes , Prognosis , Protein Interaction Maps
4.
Rev. cuba. hematol. inmunol. hemoter ; 36(3): e1243, jul.-set. 2020.
Article in Spanish | LILACS, CUMED | ID: biblio-1156443

ABSTRACT

Las neoplasias hematológicas se caracterizan por un gran número y complejidad de alteraciones genéticas, desde la formación de genes de fusión a partir de translocaciones e inversiones cromosómicas hasta mutaciones génicas y alteraciones epigenéticas que han permitido la identificación de nuevos oncogenes y genes supresores de tumores responsables de su etiología. Al abordar el estudio genético de las leucemias se utilizan múltiples técnicas como la citogenética convencional, citogenética molecular (hibridaciónin situ por fluorescencia (FISH), esta última con una mayor sensibilidad, especificidad y rapidez que permiten el diagnóstico, la estratificación pronóstica y seguimiento de la enfermedad. Las técnicas anteriores se integran con técnicas de biología molecular, secuenciación génica, entre otras, que permiten el hallazgo de nuevos marcadores genéticos con una mejor caracterización de las hemopatías malignas y la posibilidad del desarrollo de nuevos fármacos específicos que actúen sobre la diana molecular. El objetivo fue revisar la utilidad de la citogenética y la secuenciación génica en el estudio de la leucemia mieloide aguda y la leucemia linfocítica crónica. Ante las ventajas, desventajas y limitaciones de estas técnicas genéticas es necesario utilizarlas de forma complementaria y nunca excluyente(AU)


Hematological neoplasms are characterized by a large number and great complexity of genetic disorders, from the formation of fusion genes after chromosomal translocations and inversions to gene mutation and epigenetic disorders that have permitted the identification of new oncogenes and tumor-suppressing genes responsible for their etiology. When addressing the genetic study of leukemias, multiple techniques are used, such as conventional cytogenetics, molecular cytogenetics, and fluorescence in situ hybridization (FISH), the latter having the higher degree of sensitivity, specificity and speed, which allow diagnosis, prognostic stratification and follow-up of the disease. The previous techniques are integrated with molecular biology techniques, gene sequencing, among others, which allow discovery of new genetic markers with better characterization of malignant hemopathies and the possibility of developing new specific drugs against the molecular target. The objective was to review the usefulness of cytogenetics and gene sequencing in the study of acute myeloid leukemia and chronic lymphocytic leukemia. Given the advantages, disadvantages and limitations of these genetic techniques, it is necessary to use them in as complementary but never exclusive management ways(AU)


Subject(s)
Humans , Oncogenes , Genetic Markers , In Situ Hybridization, Fluorescence/methods , Hematologic Neoplasms/genetics , Cytogenetics , Epigenomics , Genetic Diseases, Inborn , Molecular Biology , Whole Genome Sequencing/methods
5.
Journal of Experimental Hematology ; (6): 2097-2012, 2020.
Article in Chinese | WPRIM | ID: wpr-880022

ABSTRACT

Enhancer of zeste homolog 2(EZH2) is a histone methyltransferase which regulate gene expression through epigenetic machinery. The abnormal expression of EZH2 has been described in many cancer types. With in-depth study, it was found that EZH2 is involved in the occurrence and development in many kinds of malignant hematologic disease which may play a dual role of oncogenes and tumor suppressor genes. In recent years, the emergence of EZH2 inhibitors provide a new option for the future treatment of hematological malignancies. In this review, the expression and clinical significance of EZH2 in various of hematological tumors were summarized briefly.


Subject(s)
Enhancer of Zeste Homolog 2 Protein/genetics , Hematologic Neoplasms/genetics , Humans , Neoplasms , Oncogenes , Research
6.
Immune Network ; : 10-2020.
Article in English | WPRIM | ID: wpr-811172

ABSTRACT

Immune checkpoint inhibitors (ICIs) have shown remarkable benefit in the treatment of patients with non-small-cell lung cancer (NSCLC) and have emerged as an effective treatment option even in the first-line setting. ICIs can block inhibitory pathways that restrain the immune response against cancer, restoring and sustaining antitumor immunity. Currently, there are 4 PD-1/PD-L1 blocking agents available in clinics, and immunotherapy-based regimen alone or in combination with chemotherapy is now preferred option. Combination trials assessing combination of ICIs with chemotherapy, targeted therapy and other immunotherapy are ongoing. Controversies remain regarding the use of ICIs in targetable oncogene-addicted subpopulations, but their initial treatment recommendations remained unchanged, with specific tyrosine kinase inhibitors as the choice. For the majority of patients without targetable driver oncogenes, deciding between therapeutic options can be difficult due to lack of direct cross-comparison studies. There are continuous efforts to find predictive biomarkers to find those who respond better to ICIs. PD-L1 protein expressions by immunohistochemistry and tumor mutational burden have emerged as most well-validated biomarkers in multiple clinical trials. However, there still is a need to improve patient selection, and to establish the most effective concurrent or sequential combination therapies in different NSCLC clinical settings. In this review, we will introduce currently used ICIs in NSCLC and analyze most recent trials, and finally discuss how, when and for whom ICIs can be used to provide promising avenues for lung cancer treatment.


Subject(s)
Biomarkers , Carcinoma, Non-Small-Cell Lung , Drug Therapy , Humans , Immunohistochemistry , Immunotherapy , Lung Neoplasms , Oncogenes , Patient Selection , Protein-Tyrosine Kinases
7.
Int. j. morphol ; 37(1): 190-195, 2019. graf
Article in English | LILACS | ID: biblio-990026

ABSTRACT

SUMMARY: Veterinary oncology is very important nowadays to get a better understanding of human carcinogenesis. Estrogen receptor, progesterone receptor and Human Epidermal Growth Factor receptor 2 are frequently evaluated by immunohistochemistry (HIC) in human breast tumor. WT1 is an oncogene, its overexpression has been detected in leukemia and diverse solid tumors like breast cancer, lung cancer and mesothelioma in humans. WT1 expression was evaluated in 15 canine breast tumors (CBT) diagnosed by histopathological analysis to find its relationship with neoplasia and malignancy. IHC and RT-PCR were performed in CBT tissues. Fisher´s test was used to analyze WT1 relationship with malignancy. Of the 15 tumors, 9 (60 %) were diagnosed as benign and 6 (40 %) were malignant. With IHC, WT1 expression was positive only in biopsies diagnosed as malignant. Expression of WT1 by RT-PCR was detected in 14 of the 15 tumors (93.33 %) as well as in control healthy mammary gland. Clinical significance: This study describes for the first time a close correlation between CBT and a positive result for WT1 expression with IHC; hence, it can be used as a biomarker for this neoplasia and as an indicator of malignancy. RT-PCR analysis also showed to be good option to detect WT1 expression. These results will be useful to further investigations to elucidate WT1-related signaling pathways in CBT. Also to know molecules that regulate the translation of this protein as a marker for tumor progression.


RESUMEN: La oncología veterinaria es muy importante hoy en día para comprender mejor la carcinogénesis humana. El receptor de estrógeno, el receptor de progesterona y el receptor 2 del factor de crecimiento epidérmico humano se evalúan con frecuencia mediante inmunohistoquímica (HIC) en tumores de mama humanos. WT1 es un oncogén, su sobreexpresión se ha detectado en leucemia y en diversos tumores sólidos como el cáncer de mama, cáncer de pulmón y mesotelioma en humanos. La expresión de WT1 se evaluó en 15 tumores de mama caninos (TCC) diagnosticados mediante análisis histopatológico para encontrar su relación con la neoplasia y la malignidad. IHC y RT-PCR se realizaron en tejidos CBT. La prueba de Fisher se utilizó para analizar la relación de WT1 con la malignidad. De los 15 tumores, 9 (60 %) fueron diagnosticados como benignos y 6 (40 %) fueron malignos. Con IHC, la expresión de WT1 fue positiva solo en biopsias diagnosticadas como malignas. La expresión de WT1 por RT-PCR se detectó en 14 de los 15 tumores (93,33 %), así como en el control de la glándula mamaria sana. Importancia clínica: este estudio describe por primera vez una estrecha correlación entre la TCC y un resultado positivo para la expresión de WT1 con IHC; por lo tanto, se puede utilizar como un biomarcador para esta neoplasia y como un indicador de malignidad. El análisis por RT-PCR también demostró ser una buena opción para detectar la expresión de WT1. Estos resultados serán útiles para futuras investigaciones para dilucidar las vías de señalización relacionadas con WT1 en la TCC. También para conocer moléculas que regulan la traducción de esta proteína como marcador de progresión tumoral.


Subject(s)
Animals , Female , Dogs , Breast Neoplasms/metabolism , Breast Neoplasms/pathology , Genes, Wilms Tumor/physiology , Oncogenes , Immunohistochemistry , Biomarkers, Tumor/metabolism , Polymerase Chain Reaction , Carcinogenesis
8.
Yonsei Medical Journal ; : 898-904, 2019.
Article in English | WPRIM | ID: wpr-762043

ABSTRACT

PURPOSE: Sonic hedgehog (Shh) signaling pathway is known to play a crucial role in carcinogenesis in various malignancies, including lung cancer regarding tumorigenesis, angiogenesis, and cellular differentiation. The aim of this study was to investigate the value of components of Shh pathway as a prognostic marker in extensive stage small cell lung cancer (ES-SCLC) patients. MATERIALS AND METHODS: We retrospectively analyzed data of 36 patients who were diagnosed with ES-SCLC between 2008 and 2012 at a single center. We performed immuo-histochemistry for glioma-associated oncogene homolog zinc finger protein 1 (Gli1), patched, Shh, and Ptch-mediated repression of smoothened (Smo) proteins using formalin-fixed, paraffin-embedded tissue derived from primary tumors. We then conducted survival analysis to evaluate the prognostic impact of these markers. RESULTS: All 36 patients received platinum-based doublet chemotherapy. The median progression free survival and median overall survival were 6.9 months [95% confidence interval (CI), 6.5–7.3] and 11.7 months (95% CI, 9.1–14.3), respectively. The overall response rate was 84%. Of the 36 tissue specimens examined, over-expression of Gli1, Patched, Shh, and Smo was found in 12 (33.3%), five (13.9%), five (13.9%), and six (16.7%) cases, respectively. We found that high expression of Shh was associated with worse progression free survival (6.3 vs. 7.6 months, p=0.005) and overall survival (9.2 vs. 12.0 months, p=0.039) by both univariate and multivariate analyses, whereas other markers were not related to patient prognosis. CONCLUSION: A high proportion of small cell lung cancer tumors express proteins related to Shh pathway, and over-expression of Shh is correlated with poor prognosis.


Subject(s)
Carcinogenesis , Disease-Free Survival , Drug Therapy , Hedgehog Proteins , Hedgehogs , Humans , Lung Neoplasms , Multivariate Analysis , Oncogenes , Prognosis , Repression, Psychology , Retrospective Studies , Small Cell Lung Carcinoma , Zinc Fingers
9.
Laboratory Medicine Online ; : 189-193, 2019.
Article in Korean | WPRIM | ID: wpr-760494

ABSTRACT

A variety of clonal cytogenetic abnormalities have been reported in aggressive natural killer (NK)-cell lymphoma and leukemia. Recent chromosomal microarray studies have shown both gain and loss of 1q and loss of 7p as recurrent abnormalities in aggressive NK-cell leukemia. Here, we report a case of aggressive NK-cell leukemia with complex chromosomal gains and losses, as confirmed by chromosomal microarray analysis. The patient showed an aggressive clinical course, which was complicated by hemophagocytic lymphohistiocytosis. Conventional cytogenetic analysis revealed trisomy 3 and 1q gain only. However, chromosomal microarray analysis detected an additional gain of 1q21.1–q24.2 and a loss of 1q24.2–q31.3. These abnormal lesions might play a role in the pathogenesis of aggressive NK-cell leukemia by inactivating tumor suppressor genes or by activating oncogenes. These results suggest that chromosomal microarray analysis may be used to provide further genetic information for patients with hematological malignancies, including aggressive NK-cell leukemia.


Subject(s)
Chromosome Aberrations , Cytogenetic Analysis , Genes, Tumor Suppressor , Hematologic Neoplasms , Humans , Leukemia , Lymphohistiocytosis, Hemophagocytic , Lymphoma , Microarray Analysis , Oncogenes , Trisomy
10.
Article in English | WPRIM | ID: wpr-764309

ABSTRACT

BACKGROUND: Helicobacter pylori infection is a major risk factor in the development of gastric cancer. H. pylori infection of gastric epithelial cells increases the levels of reactive oxygen species (ROS), activates oncogenes, and leads to β-catenin-mediated hyper-proliferation. β-Carotene reduces ROS levels, inhibits oxidant-mediated activation of inflammatory signaling and exhibits anticancer properties. The present study was carried out to determine if β-carotene inhibits H. pylori-induced cell proliferation and the expression of oncogenes c-myc and cyclin E by reducing the levels of β-catenin and phosphorylated glycogen synthase kinase 3β (p-GSK3β). METHODS: Gastric epithelial AGS cells were pre-treated with β-carotene (5 and 10 μM) for 2 hours prior to H. pylori infection and cultured for 6 hours (for determination of the levels of p-GSK3β, GSK3β, and β-catenin) and 24 hours (for determination of cell viability and protein levels of c-myc and cyclin E). Cell viability was determined by the MTT assay and protein levels were determined via western blot-based analysis. RESULTS: β-Carotene inhibited H. pylori-induced increases in the percentage of viable cells, phosphorylated GSK3β (p-GSK3β), and the levels of β-catenin, c-myc and cyclin E. CONCLUSIONS: β-Carotene inhibits H. pylori-induced hyper-proliferation of gastric epithelial cells by suppressing β-catenin signaling and oncogene expression.


Subject(s)
beta Carotene , beta Catenin , Cell Proliferation , Cell Survival , Cyclin E , Cyclins , Epithelial Cells , Glycogen Synthase Kinases , Helicobacter pylori , Helicobacter , Oncogenes , Reactive Oxygen Species , Risk Factors , Stomach Neoplasms
11.
Article in English | WPRIM | ID: wpr-764306

ABSTRACT

Medulloblastoma is considered one of the most threatening malignant brain tumors with an extremely high mortality rate in children. In the medulloblastoma, there are several genes and mutations found to work in an unregulated manner that works together to push the cells into a cancerous state. With the discovery of non-coding RNAs such as microRNAs (miRNAs), it has been shown that a different layer of gene regulations may be disrupted which would cause cancer. This fact led scientists to put their focus on the role of miRNAs in cancer. A mature miRNA contains a seed sequence which gives the miRNA to identify and attach to the interest mRNA; this attachment may lead degradation of mRNA or suppress of translation of the mRNA. The expression of miRNAs in medulloblastoma shows that some of these non-coding RNAs are overexpressed (OncomiRs) which help cells to proliferate and keep their stemness features. On the other hand, there are other forms of these miRNAs which normally inhibit cell proliferation and promote cell differentiation (tumor suppressor). These are down-regulated during cancer progression. In this systematic review, we attempted to gather several important studies on miRNAs’ role in medulloblastoma tumors and the importance of these non-coding RNAs in the future study of cancer.


Subject(s)
Brain Neoplasms , Cell Differentiation , Cell Proliferation , Child , Genes, Tumor Suppressor , Hand , Humans , Medulloblastoma , MicroRNAs , Mortality , Oncogenes , RNA, Messenger , RNA, Untranslated , Social Control, Formal
12.
Cancer Research and Treatment ; : 1207-1221, 2019.
Article in English | WPRIM | ID: wpr-763159

ABSTRACT

PURPOSE: The study aimed to search and identify genes that were differentially expressed in breast cancer, and their roles in cancer growth and progression. MATERIALS AND METHODS: The Gene Expression Omnibus (Oncomine) and The Cancer Genome Atlas databases (https://cancergenome.nih.gov/) were screened for genes that were expressed differentially in breast cancer and were closely related to a poor prognosis. Gene expressions were verified by quantitative real-time polymerase chain reaction, and genes were knocked down by a lentivirus-based system. Cell growth and motility were evaluated and in vivo nude mice were used to confirm the in vitro roles of genes. Markers of epithelial-to-mesenchymal transition and the associations of KIF11 with the classical cancer signaling pathways were detected by Western blot. RESULTS: A series of genes expressed differentially in patients with breast cancer. The prognosis associated with high KIF11 expression was poor, and the expression of KIF11 increased significantly in high stage and malignant tumor cells. Inhibiting KIF11 expression in lentivirus-suppressed cells revealed that KIF11 inhibition significantly reduced cell viability and colony formation, inhibited migration and invasion, but promoted apoptosis. The sizes and weights of KIF11-inhibited tumors in nude mice were significantly lower than in the negative controls. Western blot showed that E-cadherin in breast cancer was significantly upregulated in KIF-inhibited cells and tumor tissues, whereas N-cadherin and vimentin were significantly down-regulated. BT549 and MDA231 cells with KIF11 knockdown exhibited decreased ERK, AMPK, AKT, and CREB phosphorylation. CONCLUSION: KIF11 acts as a potential oncogene that regulates the development and progression of breast cancer.


Subject(s)
AMP-Activated Protein Kinases , Animals , Apoptosis , Blotting, Western , Breast Neoplasms , Breast , Cadherins , Cell Survival , Gene Expression , Genome , Humans , In Vitro Techniques , Mice , Mice, Nude , Oncogenes , Phosphorylation , Prognosis , Real-Time Polymerase Chain Reaction , Vimentin , Weights and Measures
13.
Natural Product Sciences ; : 298-303, 2019.
Article in English | WPRIM | ID: wpr-786431

ABSTRACT

This study investigated the cytotoxic effects and mechanism of action of asiatic acid in pancreatic cancer cell lines. First, we confirmed the cell viability of MIA PaCa-2 and PANC-1 cells after asiatic acid administration for 48 and 72 h. The viability of MIA PaCa-2 and PANC-1 cells decreased in a dose-dependent manner following asiatic acid administration. To investigate the underlying mechanism, we performed a terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay, annexin V assay, and western blotting. Asiatic acid induced apoptosis and autophagy through activation of AMP-activated protein kinase (AMPK) and inhibition of mammalian target of rapamycin (mTOR) in MIA PaCa-2 cells. Finally, the expression of miR-17 and miR-21, known as oncogenes in pancreatic cancer, was decreased by asiatic acid. These results indicate that asiatic acid has potential as a new therapeutic agent against pancreatic cancer.


Subject(s)
AMP-Activated Protein Kinases , Annexin A5 , Apoptosis , Autophagy , Blotting, Western , Cell Line , Cell Survival , DNA Nucleotidylexotransferase , MicroRNAs , Oncogenes , Pancreatic Neoplasms , Sirolimus
14.
Article in English | WPRIM | ID: wpr-785805

ABSTRACT

The incidence and mortality rate of cancer continues to gradually increase, although considerable research effort has been directed at elucidating the molecular mechanisms underlying biomarkers responsible for tumorigenesis. Accumulated evidence indicates that the long non-coding RNAs (lncRNAs), which are transcribed but not translated into functional proteins, contribute to cancer development. Recently, linc00152 (an lncRNA) was identified as a potent oncogene in various cancer types, and shown to be involved in cancer cell proliferation, invasiveness, and motility by sponging tumor-suppressive microRNAs acting as a competing endogenous RNA, binding to gene promoters acting as a transcriptional regulator, and binding to functional proteins. In this review, we focus on the oncogenic role of linc00152 in tumorigenesis and provided an overview of recent clinical studies on the effects of linc00152 expression in human cancers.


Subject(s)
Biomarkers , Carcinogenesis , Cell Proliferation , Humans , Incidence , MicroRNAs , Mortality , Oncogenes , RNA , RNA, Long Noncoding
15.
Yonsei Medical Journal ; : 336-345, 2019.
Article in English | WPRIM | ID: wpr-742550

ABSTRACT

PURPOSE: Long noncoding RNA nuclear paraspeckle assembly transcript 1 (NEAT1) has been deemed an oncogene in many human cancers. However, the underlying mechanism of NEAT1 in nasopharyngeal carcinoma (NPC) progression remains largely unclear. MATERIALS AND METHODS: Quantitative real-time PCR assay was performed to assess the expression of NEAT1 and miR-34a-5p in NPC tissues and cells. Western blot analysis was used to observe cell epithelial to mesenchymal transition (EMT) and the activation of Wnt/β-catenin signaling in 5-8F cells. MiRNA directly interacting with NEAT1 were verified by dual-luciferase reporter assay and RNA immunoprecipitation. Cell proliferation ability was determined by CCK-8 assay, and cell migration and invasion capacities were assessed by transwell assays. An animal model was used to investigate the regulatory effect of NEAT1 on tumor growth in vivo. RESULTS: Our data revealed that NEAT1 is upregulated, while miR-34a-5p is downregulated in NPC tissues and cell lines. NEAT1 knockdown repressed tumor growth in vitro and in vivo. Additionally, we discovered that NEAT1 directly binds to miR-34a-5p and suppresses miR-34a-5p expression. Moreover, NEAT1 knockdown exerted suppression effects on cell proliferation, migration, invasion, and EMT by miR-34a-5p. NEAT1 knockdown blocked Wnt/β-catenin signaling via miR-34a-5p. CONCLUSION: Our study demonstrated that NEAT1 targets miR-34a-5p at least partly to drive NPC progression by regulating Wnt/β-catenin signaling, suggesting a potential therapeutic target for NPC.


Subject(s)
Blotting, Western , Cell Line , Cell Movement , Cell Proliferation , Humans , Immunoprecipitation , In Vitro Techniques , MicroRNAs , Models, Animal , Oncogenes , Real-Time Polymerase Chain Reaction , RNA , RNA, Long Noncoding , Sincalide
16.
Rev. Univ. Ind. Santander, Salud ; 50(3): 257-268, jul.-set. 2018. tab, graf
Article in Spanish | LILACS | ID: biblio-957518

ABSTRACT

Resumen La infección crónica con virus oncogénicos es responsable de aproximadamente el 20% de todos los cánceres reportados en humanos, este proceso de oncogénesis viral presenta una naturaleza compleja, multietapa y multifactorial. Un ejemplo de ello es el Virus de Epstein- Barr (EBV), un herpesvirus que infecta de manera latente a más del 90% de la población. Aunque la infección a menudo cursa de manera asintomática, el EBV es capaz de modificar su expresión genómica estableciendo diferentes fases de latencia, alterando así el metabolismo de sus células blanco, como son los linfocitos B y las células epiteliales, proceso que resulta determinante en la aparición y desarrollo de diferentes patologías que van desde la mononucleosis infecciosa hasta procesos oncológicos como el linfoma de Burkitt, el cáncer gástrico o el cáncer nasofaríngeo.


Abstract Chronic infection with oncogenic viruses is responsible for approximately 20% of all cancers worldwide in humans, this viral transformation represents a complex, multistage and multifactorial process. An example is the Epstein-Barr virus (EBV), a herpesvirus that latently infects over 90% of the population. Although the infection often courses asymptomatically, EBV is able to modify its genomic expression by establishing different latency phases, thus altering the B lymphocytes and epithelial cells metabolism, a determinant process in the appearance and development of different pathologies ranging from infectious mononucleosis to oncological processes such as Burkitt's lymphoma, gastric cancer and nasopharyngeal cancer.


Subject(s)
Humans , Herpesvirus 4, Human , Oncogenes , Viral Proteins , Gene Expression , Virus Latency
17.
Rev. medica electron ; 40(4): 1100-1111, jul.-ago. 2018. ilus
Article in Spanish | LILACS, CUMED | ID: biblio-961283

ABSTRACT

RESUMEN La biología de los gliomas malignos se asocia con el balance de la expresión de las proteínas que controlan de manera positiva o negativa el ciclo celular, la proliferación, la motilidad, la neoformación vascular y el reconocimiento del sistema inmune. La frecuencia de las alteraciones genéticas que están presentes en GBM2 y GBM1 son diferentes así como la edad de los pacientes en la que se presentan. Mientras que los GBM1 suelen aparecer en edades más tardías, alrededor de los 60-70 años, los GBM2 suelen presentarse en edades más tempranas, 40-50 años. En la génesis del glioblastoma existen alteraciones moleculares a nivel de genes supresores de tumores, oncogenes y genes reparadores de ADN (AU).


ABSTRACT The glioblastoma it is the primary wicked tumor of the central nervous system more common in adults and it invariably associates to a bad presage. The biology of the wicked gliomas associates with the balance of the expression of the proteins that they control of positive way or negative the cellular cycle, the proliferation, the motility, the vascular neoformation and the recognition of the immune system. The frequency of the genetic alterations that they are present in GBM2 and GBM1 is different. While the GBM1 usually appears in later ages, around the 60-70 years, the GBM2 usually presents in earlier ages, 40-50 years. In the genesis of the glioblastoma exist molecular alterations at level of suppressive genes of tumors (GST), oncogenes and reparative genes of DNA (AU).


Subject(s)
Humans , Oncogenes/genetics , Biology/classification , DNA/classification , Patients , Proteins , Cell Cycle , Genes, Suppressor , Glioblastoma , Genes/genetics
18.
Annals of Coloproctology ; : 280-285, 2018.
Article in English | WPRIM | ID: wpr-718754

ABSTRACT

For many years, developmental and physiological differences have been known to exist between anatomic segments of the colorectum. Because of different outcomes, prognoses, and clinical responses to chemotherapy, the distinction between right colon cancer (RCC) and left colon cancer (LCC) has gained attention. Furthermore, variations in the molecular features and gut microbiota between right and LCCs have recently been a hot research topic. CpG island methylator phenotype-high, microsatellite instability-high colorectal cancers are more likely to occur on the right side whereas tumors with chromosomal instability have been detected in approximately 75% of LCC patients and 30% of RCC patients. The mutation rates of oncogenes and tumor suppressor genes also differ between RCC and LCC patients. Biofilm is more abundant in RCC patients than LLC patients, as are Prevotella, Selenomonas, and Peptostreptococcus. Conversely, Fusobacterium, Escherichia/Shigella, and Leptotrichia are more abundant in LCC patients compared to RCC patients. Distinctive characteristics are apparent in terms of molecular features and gut microbiota between right and LCC. However, how or to what extent these differences influence diverging oncologic outcomes remains unclear. Further clinical and translational studies are needed to elucidate the causative relationship between primary tumor location and prognosis.


Subject(s)
Biofilms , Chromosomal Instability , Colon , Colonic Neoplasms , Colorectal Neoplasms , CpG Islands , Drug Therapy , Fusobacterium , Gastrointestinal Microbiome , Genes, Tumor Suppressor , Humans , Leptotrichia , Microsatellite Repeats , Mutation Rate , Oncogenes , Peptostreptococcus , Prevotella , Prognosis , Selenomonas , Treatment Outcome
19.
Article in English | WPRIM | ID: wpr-718572

ABSTRACT

PURPOSE: Presenilins are functionally important components of γ-secretase, which cleaves a number of transmembrane proteins. Manipulations of PSEN1 and PSEN2 have been separately studied in Alzheimer disease (AD) and cancer because both involve substrates of γ-secretase. However, numerous clinical studies have reported an inverse correlation between AD and cancer. Interestingly, AD is a neurodegenerative disorder, whereas cancer is characterized by the proliferation of malignant cells. However, this inverse correlation in the PSEN double-knockout (PSEN dKO) mouse model of AD has been not elucidated, although doing so would shed light onto the relationship between AD and cancer. METHODS: To investigate the inverse relationship of AD and cancer under conditions of PSEN loss, we used the hippocampus of 7-month-old and 18-month-old PSEN dKO mice for a microRNA (miRNA) microarray analysis, and explored the tumorsuppressive or oncogenic role of differentially-expressed miRNAs. RESULTS: The total number of miRNAs that showed changes in expression level was greater at 18 months of age than at 7 months. Most of the putative target genes of the differentially-expressed miRNAs involved Cancer pathways. CONCLUSIONS: Based on literature reviews, many of the miRNAs involved in Cancer pathways were found to be known tumorsuppressive miRNAs, and their target genes were known or putative oncogenes. In conclusion, the expression levels of known tumor-suppressive miRNAs increased at 7 and 18 months, in the PSEN dKO mouse model of AD, supporting the negative correlation between AD and cancer.


Subject(s)
Alzheimer Disease , Animals , Hippocampus , Humans , Infant , Mice , Microarray Analysis , MicroRNAs , Neurodegenerative Diseases , Oncogenes , Presenilins
20.
Yonsei Medical Journal ; : 1143-1149, 2018.
Article in English | WPRIM | ID: wpr-718498

ABSTRACT

Various molecular targeted therapies and diagnostic modalities have been developed for the treatment of hepatocellular carcinoma (HCC); however, HCC still remains a difficult malignancy to cure. Recently, the focus has shifted to cancer metabolism for the diagnosis and treatment of various cancers, including HCC. In addition to conventional diagnostics, the measurement of enhanced tumor cell metabolism using F-18 fluorodeoxyglucose (18F-FDG) for increased glycolysis or C-11 acetate for fatty acid synthesis by positron emission tomography/computed tomography (PET/CT) is well established for clinical management of HCC. Unlike tumors displaying the Warburg effect, HCCs vary substantially in terms of 18F-FDG uptake, which considerably reduces the sensitivity for tumor detection. Accordingly, C-11 acetate has been proposed as a complementary radiotracer for detecting tumors that are not identified by 18F-FDG. In addition to HCC diagnosis, since the degree of 18F-FDG uptake converted to standardized uptake value (SUV) correlates well with tumor aggressiveness, 18F-FDG PET/CT scans can predict patient outcomes such as treatment response and survival with an inverse relationship between SUV and survival. The loss of tumor suppressor genes or activation of oncogenes plays an important role in promoting HCC development, and might be involved in the “metabolic reprogramming” of cancer cells. Mutations in various genes such as TERT, CTNNB1, TP53, and Axin1 are responsible for the development of HCC. Some microRNAs (miRNAs) involved in cancer metabolism are deregulated in HCC, indicating that the modulation of genes/miRNAs might affect HCC growth or metastasis. In this review, we will discuss cancer metabolism as a mechanism for treatment resistance, as well as an attractive potential therapeutic target in HCC.


Subject(s)
Carcinoma, Hepatocellular , Diagnosis , Drug Resistance , Electrons , Fluorodeoxyglucose F18 , Genes, Tumor Suppressor , Glycolysis , Humans , Metabolism , MicroRNAs , Molecular Targeted Therapy , Neoplasm Metastasis , Oncogenes , Positron Emission Tomography Computed Tomography
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