Objective: The research paid close attention to the function of lncRNA-related endogenous competitive RNAs (ceRNAs) network in endometrial cancer (EC). Methods: 45 primary endometrial cancer tissues (EC) and 45 normal endometrium (NE) were included in the research. The online software StarbaseV2.0 was made use of forecasting the lncRNA which most likely contained microRNA-200c-3p combining sites and could interact with microRNA-200c-3p. Subsequently, we chose lncRNAs which were consistent with the characteristics of polyadenylation of lncRNAs and lower expression in EC than that of NE. After that, lncRNAs, which were related with the microRNA-200c-3p-noxa network, were identified. Results: Rp11-379k17.4, a new gene related to endometrial cancer, was identified as noncoding RNA. It was a more effective ceRNA associated with the microRNA-200c-3p-noxa network. Conclusion: LncRNAs possess microRNA response elements (MREs) and give scope to significant roles in the post-transcriptional mechanism in EC.

The aim of the present study was to determine the competitive endogenous RNA (ceRNA) network associated with long-coding RNA (lncRNA) LA16c-313D11.11 in endometrial cancer (EC). Initially, the expression levels of LA16c-313D11.11 in 60 EC tissues, 20 atypical hyperplasia endometrium (EAH) tissues and 20 normal endometrium tissues was determined. MicroRNA (miRNA/miR)-205-5p mimics and LA16c-313D11.11 mimics were transfected into HEC-1A and Ishikawa cells. The expression levels of miR-205-5p, LA16c-313D11.11 and their target proteins were assessed using reverse transcription-quantitative PCR or western blot analysis. Flow cytometry, Cell Counting kit-8 assays, Transwell migration assays and wound healing assays were performed to assess the effects of LA16c-313D11.11 and miR-205-5p on the migration and proliferation of tumor cells in vitro. The expression levels of LA16c-313D11.11 and phosphatase and tensin homolog deleted on chromosome ten (PTEN) in human EAH and EC tissues were significantly decreased, whereas the expression levels of miR-205-5p in EAH and EC tissues were significantly increased, compared with the normal endometrium tissues. The expression of LA16c-313D11.11 in human EC tissues negatively correlated with the expression of miR-205-5p. Additionally, the overexpression of LA16c-313D11.11 significantly reduced the invasion, migration and viability of HEC-1A and Ishikawa cells in vitro. LA16c-313D11.11 was shown to regulate the expression of PTEN, and the invasion, migration and viability of HEC-1A and Ishikawa cells, through its microRNA response element to compete for microRNA-205-5p. LA16c-313D11.11 was also shown to modulate the PI3K/AKT signaling pathway. Therefore, LA16c-313D11.11 acts as an effective ceRNA associated with a microRNA-205-5p-PTEN axis. LA16c-313D11.11 may inhibit the development and progression of EC by acting as a sponge of miR-205-5p, thus indirectly increasing the expression of PTEN.

The long noncoding RNA (lncRNA) H19 is involved in the pathogenesis of endometriosis by modulating the proliferation and invasion of ectopic endometrial cells in vitro , but related in vivo studies are rare. This study aimed to investigate the role of lncRNA H19 in a nude mouse model of endometriosis. Ectopic endometrial stromal cells (ecESCs) were isolated from ectopic endometrium of patients with endometriosis and infected with lentiviruses expressing short hairpin RNA (shRNA) negative control (LV-NC-shRNA) or lncRNA-H19 shRNA (LV-H19-shRNA). The ecESCs infected with LV-NC-shRNA and LV-H19-shRNA were subcutaneously implanted into forty 6- to 8-week-old female nude mice. The size and weight of the endometriotic implants were measured at 1, 2, 3, and 4 weeks after implantation and compared, and lncRNA H19 levels in endometriotic implants were evaluated using real-time polymerase chain reaction (RT-PCR). All nude mice survived the experimental period, and no significant differences in body weight were observed between the experimental group and the control group. All nude mice developed histologically confirmed subcutaneous endometriotic lesions with glandular structures and stroma after 1 week of implantation. The subcutaneous lesions in the LV-NC-shRNA group after 1, 2, 3, and 4 weeks of implantation were larger than those in the LV-H19-shRNA group, and lncRNA H19 levels in subcutaneous lesions in the LV-NC-shRNA group were significantly higher than those in the LV-H19-shRNA group. Knockdown of lncRNA H19 suppresses endometriosis in vivo . Further study is required to explore the underlying mechanism in the future.

Long non-coding RNAs (lncRNAs) represent a class of versatile molecules that exhibit the potential to regulate gene expression at various levels, namely transcriptional, post-transcriptional and epigenetic, thereby influencing critical cellular processes such as proliferation, apoptosis, invasion and drug resistance. The lncRNA H19, among the earliest identified within this category, has emerged as a significant participant in the pathogenesis of a multitude of both malignant and benign gynecological diseases. An escalating body of evidence indicates a functionally pertinent network of lncRNA H19 coexpression linked with the extracellular matrix architecture and immune microenvironment during cancer progression. This association may provide insightful leads for the selection of innovative diagnostic biomarkers and assist in the delineation of potent pharmaceutical targets for gynecological oncology. The present comprehensive review presented a synthesis of the expression profiles and multifaceted implications of lncRNA H19 across a spectrum of gynecological pathologies. Contents1. Introduction 2. Overview of lncRNA 3. Multifaceted role of lncRNA H19 4. lncRNA H19 and gynecologic malignancies 5. lncRNA H19 and benign gynecological diseases 6. Effects of lncRNA H19 on immunity 7. Conclusion

Preoperative oil administration is a feasible and effective method to display the chylous tubes and to prevent the chylous leakage in para-aortic lymphadenectomy.