Exploring the Effects of Various Early Hospital Feeding Approaches on Feeding Tolerance and Growth in Premature Infants.

Background: Feeding intolerance poses a significant risk of malnutrition in premature infants and may result in postnatal growth restriction, leading to irreversible damage to brain function and structure. Objective: This study aims to investigate the impact of various early hospital feeding methods on feeding tolerance and the early growth and development of premature infants. Design: A retrospective study design was adopted in this study. Setting: This study was conducted at Tongling Maternal and Child Health Hospital between January 2018 and June 2023. Participants: A total of premature, low birth-weight infants admitted to our hospital between January 2018 and June 2023 were selected for the study. The preterm infants were randomly assigned to either the experimental group (EG) or the control group (CG) using the random number table method. Interventions: The EG group received deep hydrolyzed protein formula (DHPF) milk for 1-3 weeks after opening, whereas the CG group received preterm infant formula milk continuously after the milk was opened. Primary Outcome Measures: (1) Growth and development, (2) Feeding tolerance, and (3) Incidence of complications. Results: Following 14 days of feeding, both study groups exhibited notable increases in body length, body weight, and head circumference (P < .05). These measurements were significantly higher in the EG compared to the CG (P < .05). Furthermore, the EG demonstrated a marked improvement in feeding tolerance relative to the CG (P < .01). Notably, there was no significant difference in the incidence of complications between the two groups (P > .05). Conclusions: The administration of deep hydrolyzed protein formula (DHPF) milk presents a promising strategy for enhancing the growth and development of premature infants while concurrently improving feeding tolerance. These findings underscore the potential clinical benefits of incorporating DHPF milk into neonatal care protocols.

Antifouling Electrochemiluminescence Biosensor Based on Bovine Serum Albumin Hydrogel for the Accurate Detection of p53 Gene in Human Serum.

To detect biomarkers in complex samples, it is fundamental to avoid the nonspecific adsorption of impurities to improve the selectivity of biosensors. In this study, a sensitive antifouling electrochemiluminescence biosensor was proposed based on bovine serum albumin (BSA)- and exonuclease III (Exo III)-mediated nucleic acid cycle signal amplification strategy. Ti3C2Tx-NH4, which has a large surface area and high metal conductivity, was crosslinked with BSA to improve the conductivity of the sensing interface, which shows antifouling performance excellently due to the electrical neutrality and good hydrophilicity of BSA hydrogel. The cyclic amplification strategy based on Exo III and DNA hybridization chain reaction significantly amplified the electrochemiluminescence signal and improved the sensitivity of p53 gene detection. The linear range of the biosensor is 1 fM-1 nM with a detection limit of 0.26 fM. More importantly, the sensor showed excellent selectivity when it was used to detect the p53 gene in real samples, such as serum. Thus, this unique antifouling sensing interface is expected to construct various electrochemical biosensors in clinical diagnosis and biopathological analysis.

RBM15 m6 A modification-mediated OTUB2 upregulation promotes cervical cancer progression via the AKT/mTOR signaling.

Cervical cancer (CC) is a deadly gynecological tumor worldwide. Otubain 2 (OTUB2) has been recently identified as an oncogene in human malignancies. However, its expression and function remain unclear. This work aims to explore the role of OTUB2 in CC progression. Herein, The Cancer Genome Atlas data revealed that OTUB2 expression was significantly upregulated in cervical squamous cell carcinoma and endocervical adenocarcinoma (CESC) and gradually increased with CESC progression; moreover, OTUB2 expression predicted poor outcomes of CESC patients. Then, RT-qPCR and Western blotting were applied to determine mRNA and protein expression in CC and normal cells. Our results confirmed that OTUB2 was highly expressed in CC cell lines. As indicated by CCK-8, Transwell, and flow cytometry results, OTUB2 silencing attenuated proliferative and metastatic capacities of CC cells but promoted CC cell apoptosis. Then, RBM15, an N6-methyladenosine (m6 A) methyltransferase "writer," was also demonstrated to be upregulated in CESC and CC cells. Mechanistically, m6 A RNA immunoprecipitation (Me-RIP) results showed that RBM15 inhibition reduced the m6 A methylation level of OTUB2 in CC cells, leading to the decline of OTUB2 expression. In addition, OTUB2 inhibition deactivated the AKT/mTOR signaling in CC cells. Furthermore, SC-79 (AKT/mTOR activator) partially abated the inhibitory effects of OTUB2 knockdown on the AKT/mTOR signaling pathway and the malignant phenotypes of CC cells. In summary, this work showed that RBM15-mediated m6 A modification led to OTUB2 upregulation, thereby promoting malignant behaviors of CC cells via the AKT/mTOR signaling pathway.

The mechanism of BRCC3/NLRP3 in promoting the transformation of endometriosis to endometriosis-associated ovarian carcinoma / 中国肿瘤生物治疗杂志

@#[摘 要] 目的：探讨NOD样受体蛋白3（NLRP3）炎症小体的活化在子宫内膜异位症（EMT）进展为EMT相关性卵巢癌（EAOC）过程中的作用及其机制。方法：选取2018年4月至2019年6月上海市长宁区幼保健院收治的EAOC、EMT、正常子宫内膜（CON组）组织标本各15例及患者的临床资料，利用免疫组织化学染色法、WB法检测EAOC、EMT和CON组织中NLRP3、caspase-1和IL-1β及含BRCA1/BRCA2的复杂亚基3（BRCC3）的表达水平。构建过表达BRCC3质粒和si-NLRP3质粒并转染EMT细胞CRL-7566，通过WB法检测转染后细胞中BRCC3蛋白的表达水平，利用MTT法、流式细胞术及Transwell实验分别检测转染后细胞增殖、凋亡、迁移与侵袭能力的变化。对过表达BRCC3组细胞进行干扰NLRP3实验，通过WB法检测干扰后BRCC3和NLRP3蛋白的表达水平，检测干扰后细胞增殖、凋亡、迁移与侵袭能力的变化。结果：EAOC和EMT组织中NLRP3、caspase-1、IL-1β和BRCC3的表达水平较CON组均呈明显升高（均P<0.01），且EAOC组织中NLRP3与BRCC3的表达呈正相关（r=0.65，P<0.01）。在CRL-7566细胞中过表达BRCC3显著促进细胞的增殖、迁移和侵袭并抑制细胞凋亡（均P<0.01），敲减NLRP3则抑制CRL-7566细胞的上述表型（均P<0.01），过表达BRCC3增强NLRP3的表达水平（P<0.01），而干扰BRCC3则抑制NLRP3表达（P<0.01）；干扰NLRP3可以部分逆转BRCC3对细胞凋亡的抑制作用（P<0.01）、对细胞迁移（P<0.05）和侵袭（P<0.01）的促进作用。结论：EAOC和EMT组织中NLRP3和BRCC3均呈高表达，过表达BRCC3可促进CRL-7566细胞的增殖、迁移和侵袭并抑制细胞凋亡，与EMT向EAOC转化有关，BRCC3/NLRP3是潜在的EAOC炎癌转化预测标志物及治疗靶点。

Life Modifications and PCOS: Old Story But New Tales.

Polycystic ovary syndrome (PCOS) is defined as a kind of endocrine and metabolic disorder that affects female individuals of reproductive age. Lifestyle modifications, including diet modifications, exercise, and behavioral modification, appear to alleviate the metabolic dysfunction and improve the reproductive disorders of PCOS patients (particularly in obese women). Therefore, lifestyle modifications have been gradually acknowledged as the first-line management for PCOS, especially in obese patients with PCOS. However, the mechanism of lifestyle modifications in PCOS, the appropriate composition of diet modifications, and the applicable type of exercise modifications for specific female populations are rarely reported. We conducted a systematic review and enrolled 10 randomized controlled trials for inclusion in a certain selection. In this review, we summarized the existing research on lifestyle modifications in PCOS. We aimed to illustrate the relationship between lifestyle modifications and PCOS (referring to hyperandrogenism, insulin resistance as well as obesity) and also considered the priorities for future research. These results might be an invaluable tool to serve as a guide in lifestyle modifications as the intervention for PCOS and other related endocrine disorders.

Gut and Vaginal Microbiomes in PCOS: Implications for Women's Health.

PCOS is defined as a kind of endocrine and metabolic disorder which affects females at reproductive ages, is becoming much more common, nowadays. Microbiomes are known as microorganisms that inhabit the body to play a vital role in human health. In recent years, several basic and clinical studies have tried to investigate the correlation between the reproductive health/disorder and microbiomes (gut microbiomes and vaginal microbiomes). However, the mechanism is still unclear. In this review, we reviewed the relationship between PCOS and microbiomes, including gut/vaginal microbiomes compositions in PCOS, mechanism of microbiomes and PCOS, and then collectively focused on the recent findings on the influence of microbiomes on the novel insight regarding the therapeutic strategies for PCOS in the future clinical practice.

LncRNA HOTAIR Promotes Chemoresistance by Facilitating Epithelial to Mesenchymal Transition through miR-29b/PTEN/PI3K Signaling in Cervical Cancer.

Long non-coding RNA HOTAIR has been revealed to participate in the tumorigenesis of various cancers. However, the mechanism of HOTAIR involvement in cervical cancer has not been identified. Hence, this study aimed to explore the oncogenic and chemoresistant roles of HOTAIR in cervical cancer, and its underlying mechanism. RT-PCR, Western blot, and Luciferase assay were employed to determine the relationship of HOTAIR with miR-29b and PTEN and to study the role of HOTAIR in cervical cancer. CCK8 assay, cell migration, and invasion assay were used to reveal the role of HOTAIR in cervical cancer cell proliferation and metastasis. The inhibitory dose of chemotherapeutics was determined by CCK8 assay using probit analysis. HOTAIR was found to bind with miR-29b, and a negative correlation existed between HOTAIR and miR-29b expression in cervical cancer cells. In addition, HOTAIR promoted the migration and proliferation of cervical cancer cell lines HeLa and Siha, showing effects opposite to miR-29b. Further, HOTAIR facilitated the resistance of both HeLa and Siha cells against cisplatin, paclitaxel and docetaxel, whereas miR-29 suppressed the resistance of both cervical cancer cells against the 3chemotherapeutics. In addition, HOTAIR enhanced epithelial-to-mesenchymal transition (EMT), while miR-29b exerted an inhibitory effect on EMT. In cervical cancer cells, miR-29b did not affect promoter methylation of PTEN but regulated PTEN expression by targeting SP1. Transfection of miR-29b mimics led to a significant downregulation of PI3K. HOTAIR promotes chemoresistance by facilitating EMT through the miR-29b/PTEN/PI3K axis in cervical cancer.

A Modified Technique of Bipolar Loop Resectoscopic Slicing for Treating Submucous Fibroids With Enucleation Makes the Operation Safer.

Background: In this study, a modified technique of resectoscopic slicing with a common bipolar loop was introduced, which facilitated the complete removal of the submucous fibroid inside the uterine cavity without any novel equipment. Results: Compared with the classical technique, our modified procedure possessed a shorter operation time (22.9 ± 7.3 vs. 38.9 ± 13.0 min, p < 0.05) and a smaller distending media volume (1,495.6 ± 540.1 vs. 2,393.1 ± 719.4 ml, p < 0.01). Conclusion: As a result, the current study suggested that the enucleation of submucous fibroid under hysteroscopy could be achieved by using only the bipolar loop, which reduced the consumption for novel equipment and enhanced the safety of the technique.

HOTAIR Contributes to Stemness Acquisition of Cervical Cancer through Regulating miR-203 Interaction with ZEB1 on Epithelial-Mesenchymal Transition.

Cervical cancer stem cells contribute respond to considerable recurrence and metastasis of patients with cervical cancer. The stemness properties were partly regulated by the interaction of lncRNAs and miRNAs. HOTAIR functions as an oncogenic lncRNA. Previous research studies revealed its role in regulating stemness properties in various cancers. However, the role of HOTAIR in cervical cancer stem cells is still unknown. Here, cisplatin-resistant and serum-free cultured cells exhibited stem cells properties. Cervical cancer stem cells exhibited greater invasion and migration compared with their parental cells, which was similar to cells overexpressing HOTAIR. HOTAIR was significantly overexpressed in cervical cancer stem cells, and knockdown of HOTAIR generated statistical downregulation of stemness markers. Additionally, HOTAIR expression was negatively correlated with the level of miR-203, which was found to be an inhibitory miRNA in regulating the expressions of stemness markers. Also, miR-203 expression was negatively correlated with ZEB1. These findings suggested that HOTAIR should be a positive contributor in stemness acquisition of cervical cancer cells, and this effect should correlate with the interaction with miR-203, which can be suppressed by ZEB1.

Histone deacetylase 1 facilitates aerobic glycolysis and growth of endometrial cancer.

The deregulation of histone deacetylase 1 (HDAC1) is reportedly involved in the progression of several cancer types. However, its function in endometrial cancer remains unknown. The aim of the present study was to clarify the role of HDAC1 in aerobic glycolysis and the progression of endometrial cancer. Lentiviral vector transfection was used to up- and downregulate HDAC1 expression in HEC-1-A endometrial cancer cells. The effects of HDAC1 on cellular proliferation, apoptosis, migration, invasiveness and tumorigenesis were determined by CCK-8, flow cytometry, wound-healing, transwell chamber and in vivo tumor formation experiments, respectively. HDAC1 level was significantly increased in endometrial cancer tissues and cells, and its high expression was associated with advanced clinicopathological progression. HEC-1-A cell proliferation, invasiveness, migration and tumorigenesis were enhanced, and apoptosis was inhibited when HDAC1 was overexpressed. Moreover, upregulation of HDAC1 significantly promoted the epithelial-mesenchymal transition of HEC-1-A cells, and increased glucose consumption, lactate secretion and ATP levels. Collectively, the present study revealed that HDAC1 promoted the aerobic glycolysis and progression of endometrial cancer, which may provide a potential target for endometrial cancer treatment.

Comprehensive Analysis of circRNA-miRNA-mRNA Network in Cervical Squamous Cell Carcinoma by Integrated Analysis.

PURPOSE: Cervical squamous cell carcinoma (CSCC) seriously affects women's health worldwide, and it is of great significance to illuminate the specific role of circRNAs in CSCC. MATERIALS AND METHODS: Three mRNA datasets, two miRNA datasets and one circRNA dataset of CSCC, downloaded from GEO, were utilized in this study. Differentially expressed mRNAs (DEmRNAs), miRNAs (DEmiRNAs) and circRNAs (DEcircRNAs) were identified, and a ceRNA (DEcircRNA-DEmiRNA-DEmRNA) regulatory network was constructed. GO and pathway analyses of DEcircRNAs and DEmRNAs in the ceRNA regulatory network were performed. Quantitative real-time polymerase chain reaction (qRT-PCR) validation of the expression of the selected DEmRNAs, DEmiRNAs and DEcircRNAs was performed. RESULTS: A total of 1356 DEmRNAs, 13 DEmiRNAs and 77 DEcircRNAs were obtained. The ceRNA network contained 3 circRNA-miRNA pairs and 158 miRNA-mRNA pairs, including 3 circRNAs, 3 miRNAs, and 138 mRNAs. Functional annotation of DEmRNAs in the ceRNA regulatory network revealed that these DEmRNAs were significantly enriched in cell cycle, p53 signalling pathway and DNA replication. The qRT-PCR results were generally consistent with those of our integrated analysis. CONCLUSION: In conclusion, we speculate that the regulation of the hsa_circ_0000069/hsa-miR-125b-5p/CDKN2A and hsa_circ_0020594/hsa-let-7c-5p/CCNB2 axes may be involved in CSCC.

MiR-369-3p participates in endometrioid adenocarcinoma via the regulation of autophagy.

BACKGROUND: The aim of this study is to examine miRNA profiling and miR-369-3p participates in endometrioid adenocarcinoma (EEC) via the regulation of autophagy. METHODS: EEC and its adjacent normal tissues were obtained from 20 clinical patients after surgery. MiRNA profiling was performed using next generation sequencing (NGS) and was validated with quantitative real time PCR (qRT-PCR). qRT-PCR was also employed to measure miR-369-3p and autophagy-related protein 10 (ATG10) expression levels. Western blotting assay was performed to measure the expressions of ATG10 and LC3B. Luciferase reporter assay was conducted to confirm the direct targeting of ATG10 by miR-369-3p. Cell proliferation and migration assays were utilized to analyze the role of miR-369-3p in HEC-1-A cells. RESULTS: We found that miR-369-3p expression levels were down-regulated in EEC compared to the control tissues. The overexpression of miR-369-3p inhibited cell proliferation and migration in EEC; furthermore, ATG10 expression increased in EEC tissues. ATG10 was found to be a potential target of miR-369-3p via a dual-luciferase reporter assay, and ATG10 was shown to be down-regulated by miR-369-3p in protein levels. CONCLUSIONS: This study revealed that miR-369-3p inhibited cell proliferation and migration by targeting ATG10 via autophagy in EEC.

The Clearance of High-Risk Human Papillomavirus is Sooner After Thin Loop Electrosurgical Excision Procedure (t-LEEP).

Purpose/aim of the study: To investigate high-risk human papillomavirus (HPV) infection clearance following thin loop electrosurgical excision procedure (t-LEEP) among patients with cervical benign lesion. Materials and Methods: This retrospective study analyzed clinical data from patients with cervical benign lesion and HPV infection, who had undergone t-LEEP (T-Group), compared with patients with HPV infection undergone no treatment (NT-Group). Both groups attended regular follow-up between January 2008 and January 2012. Kaplan-Meier analysis was used to compare the HPV clearance time. Results: The average clearance time was 7.7 months (M) (95% confidence interval [CI]: 6.5-8.9 M) in T-Group, and 10.4 M (95%CI: 9.4-11.3 M) in NT-Group, with significant difference between groups (p = 0.003). Among patients with low viral load, the HPV clearance times were 7.6 M (95%CI: 6.3-9.0 M) in T-Group and 9.7 M (95%CI: 8.6-10.8 M) in NT-Group (p = 0.042). Among patients with high viral load, the HPV clearance times were 8.0 M (95%CI: 5.3-10.6 M) in T-Group and 11.4 M (95%CI: 9.7-13.1 M) in NT-Group (p = 0.041). The average time of HPV clearance in T-Group was shorter than NT-Group in all age groups, with significant differences in ≤29Y-group (p = 0.008) and 30-39Y-group (p = 0.005). The accumulated clearance rate of HPV infection at sixth month and 12th month were 24.5% and 67.9% in T-Group, 7.8% and 43.1% in NT-Group, with significant differences (p = 0.001 at 6th month, p = 0.032 at 12th month). Conclusions: T-LEEP accelerates the clearance of high-risk HPV infection and make the HPV infection rates dropped rapidly in the first year.

AKIP1 promotes angiogenesis and tumor growth by upregulating CXC-chemokines in cervical cancer cells.

Upregulation of A-kinase-interacting protein 1 (AKIP1) has been observed in breast and esophageal cancers, indicating that AKIP1 may be a potent oncogenic protein. However, the role of AKIP1 in cervical cancer still remains unknown. This study aimed to explore the role of AKIP1 in cervical cancer and to investigate the underlying mechanism of AKIP1 in tumor growth. Expression of AKIP1 in cervical cancer cells was determined by qRT-PCR and western blotting. Cell-Light EdU and colony formation assays were used to determine cell proliferation. CXCL1 and CXCL8 proteins were quantified by ELISA kits. Western blotting and qRT-PCR were used to examine the alterations in signaling-related proteins and mRNA, respectively. Endothelial cell tube formation assay was performed to evaluate the effect of AKIP1 on angiogenesis. A BALB/c nude mouse xenograft model was used to evaluate the role of AKIP1 in vivo. Cancer cell proliferation was inhibited and tumor growth and angiogenesis restrained in BALB/c nude mice by suppressing AKIP1 expression in cervical cancer cell lines. In addition, overexpression of AKIP1 in cervical cancer cells elevated the levels of CXCL1, CXCL2, and CXCL8. These three chemokines were not only involved in endothelial tube formation by binding to the endothelial receptor CXCR2, but also in cervical cancer cell proliferation and clone formation, which were induced by overexpression of AKIP1. Furthermore, we found that AKIP1-induced chemokine expression was decreased by an inhibitor of nuclear factor kappa-B kinase subunit ß. These results show that AKIP1 is crucial in cervical cancer angiogenesis and growth by elevating the levels of the NF-κB-dependent chemokines CXCL1, CXCL2, and CXCL8.

Identification of a microRNA signature associated with survivability in cervical squamous cell carcinoma.

BACKGROUND: The aim of this study is to find the potential miRNA expression signature capable of predicting survival time for cervical squamous cell carcinoma (CSCC) patients. METHODS: The expression of 332 miRNAs was measured in 131 (Training cohort) and 130 (Validation cohort) patients with CSCC in the Cancer Genome Atlas (TCGA) data portal. The miRNA expression signature was identified by Cox Proportion Hazard regression model to the Training data set, and subsequently validated in an independent Validation set. Kaplan-Meier curves and the receiver operating characteristic analyses of 5 years were used to access the overall survival of miRNA signature. MiRNA signature-gene target analysis was performed, followed by the construction of the regulatory network. Gene Ontology and Kyoto Encyclopedia of Genes and Genomes pathway analysis were used to explore the function of target genes of miRNA signature. RESULTS: A 2-miRNA expression signature of hsa-mir-642a and hsa-mir-378c associated with survivability was identified in CSCC. Both of them had a significant diagnostic and prognostic value of patients with CSCC. A total of 345 miRNA signature-target pairs were obtained in the miRNA signature-gene target regulatory network, in which 316 genes were targets of has-mir-378c and has-mir-642a. Functional analysis of target genes showed that MAPK signaling pathway, VEGF signaling pathway and endocytosis were the significantly enriched signal pathways that covered most genes. CONCLUSIONS: The 2-miRNA signature adds to the prognostic value of CSCC. In-depth interrogation of the 2-miRNAs will provide important biological insights that finding and developing novel molecularly prediction to improve prognosis for CSCC patients.

MicroRNA-23a regulates epithelial-to-mesenchymal transition in endometrial endometrioid adenocarcinoma by targeting SMAD3.

BACKGROUND: To investigate the role of total cellular microRNA (miRNA) in regulating epithelial-to-mesenchymal transition (EMT) during human endometrial endometrioid adenocarcinoma (EEC). METHODS: A miRCURY LNA microRNA array was used to evaluate the miRNA profiles of human EEC tissues and corresponding nontumorous endometriums. An in vitro model of TGF-ß induced EMT in HEC-1-A cells was used to investigate the role of miRNAs in the EEC during EMT. The expression of SMAD3, SMAD5, and a panel of EMT markers was detected by Western blot and quantitative PCR. RESULTS: The results of miRNA profiling in human EEC tissues and corresponding nontumorous endometriums demonstrated that miR-23a expression was down-regulated. Using bioinformatics, we identified SMAD3 or SMAD5 maybe as a predicted target of miR-23a. The results of luciferase reporter assay showed miR-23a directly targets and down-regulates human SMAD3 protein levels, not SMAD5 protein levels. Furthermore, overexpression of miR-23a in HEC-1-A cells increased E-cadherin expression and decreased the expression of vimentin and alpha smooth muscle actin, markers of mesenchymal cellular phenotype. CONCLUSIONS: Our data provide firm evidence of a role for miR-23a in the direct regulation of EMT through its targeting of SMAD3. Due to its ability to repress the EMT, miR-23a may be a novel target for EER therapeutic intervention.

Molecular mechanisms underlying endometriosis pathogenesis revealed by bioinformatics analysis of microarray data.

OBJECTIVE: To identify differentially expressed genes (DEGs) in endometriosis and further analyze molecular mechanisms implicated in disease pathogenesis. MATERIALS AND METHODS: Gene expression data (ID: GSE7846) of human endometrial endothelial cells (HEECs) collected from eutopic endometria tissue of patients with and without endometriosis were downloaded from Gene Expression Omnibus. DEGs were screened using Limma package, followed by enrichment analysis using clusterProfiler package in R. Thereafter, protein-protein interactions (PPIs) were analyzed using STRING (Search Tool for the Retrieval of Interacting Genes) database and visualized by Cytoscape software. Meanwhile, transcription factors were screened from the DEGs based on TRANSFA database, followed by construction of regulatory network using Cytoscape. RESULTS: A total of 2255 up- and 408 down-regulated genes were identified in endometriosis patients as compared with control patients. Those DEGs were predominantly enriched in focal adhesion (e.g., FN1, EGF, FYN, EGFR, RAC1, CCND1 and JUN), regulation of actin cytoskeleton (e.g., FN1, EGF, EGFR, RAC1 and JUN) and MAPK signaling pathway (e.g., EGF, EGFR, RAC1, JUN, TGFB1 and MYC). Importantly, EGF, EGFR, JUN, FN1, RAC1, TGFB1, CCND1 and FYN were hub nodes in the PPI network. Additionally, TGFB1, SMAD1 and SMAD4 showed up-regulation in TGFB signaling pathway. Transcription factor MYC had a regulatory effect on the most DEGs, including TGFB1, RAC1 and CCND1. CONCLUSIONS: Focal adhesion, regulation of actin cytoskeleton, MAPK and TGFB/SMAD signaling pathway may be important molecular mechanism underlying the pathogenesis of endometriosis.

Mir-155 promotes cervical cancer cell proliferation through suppression of its target gene LKB1.

MicroRNAs (miRNAs) are important regulators of many physiological and pathological processes, including cell proliferation, apoptosis, and cell cycle arrest. In this study, we aimed to investigate the biological role of miR-155 in cervical cancer and the underlying molecular mechanism involved in tumorigenesis. The expression of miR-155 in human cervical cancer tissues was detected by real-time PCR. MTT assay and BrdU incorporation assay were used to measure the proliferation of cervical cancer cells. Apoptosis cells and cell cycle distribution were analyzed by flow cytometry. We found that the expression of miR-155 was upregulated in cervical cancer tissues compared to the adjacent non-cancer tissues. Overexpression of miR-155 promoted the proliferation of Hela and SiHa cells. By contrast, downregulation of miR-155 inhibited the growth of cervical cancer cells. Flow cytometry analysis showed that low expression of miR-155 promoted apoptosis and induced cell cycle arrest in Hela and SiHa cells. Moreover, the mRNA and protein expression of LKB1 was significantly reduced in cervical cancer tissues. Luciferase reporter assay demonstrated that LKB1 was a target gene of miR-155, suggesting that miRNA-155 promoted the proliferation of cervical cancer cells by regulating LKB1 expression.