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OBJECTIVE To evaluate the efficiency, postoperative hysterectomy rate, and influencing factors for therapeutic effect of the NovaSure endometrial ablation procedure in abnormal uterine bleeding (AUB). METHODS We conducted a retrospective cohort study of 2152 patients from the Department of Gynecology at the Third Xiangya Hospital, CSU from October 2010 to December 2018. RESULTS From the first year to the eighth year after operation, annual effective rate was above 95.24%, and the differences were not statistically significant. There are statistically significant differences between the effective and ineffective groups with regard to age, intrauterine polyps, total length of the uterus, systemic coagulation disorder, and preoperative hemoglobin. A multivariate logistic regression analysis showed that the risk factors associated with systemic coagulation disorders (P = 0.027) and high total uterine length (P = 0.003) affected NovaSure efficacy in the treatment of AUB. By December 2019, the postoperative hysterectomy rate was 1.86% (40/2152) and the complication rate was 1.67% (36/2152). CONCLUSION NovaSure is a reliable treatment for AUB and serious medical complications because of its simple operation, low amount of bleeding, quick postoperative recovery, and safe and effective short-term and long-term efficacy. However, it should be carefully selected for patients with a total uterus length exceeding 10 cm.

Objective Epithelial ovarian cancer (EOC) is a common gynecologic malignancy characterized by extensive peritoneal metastasis and high mortality rate. ABHD11 Antisense RNA1 (ABHD11‐AS1) has recently been identified as a regulator of growth and metastasis in multiple tumors, including EOC. However, the biological function and potential mechanism of ABHD11‐AS1 in EOC remains poorly understood. Methods Immunohistochemistry, western blot, and qRT‐PCR analysis were used to determine the expression pattern of ABHD11‐AS1 and epidermal growth factor receptor (EGFR) in both EOC tissues and cell lines, respectively. Colony formation, transwell and wound healing assays were performed to evaluate the roles of EGFR and ABHD11‐AS1 on the capacity of cell proliferation, migration, and invasion. Western blot analysis was performed to measure the regulation of EGFR pathway on STAT3. Moreover, chromatin immunoprecipitation was employed to demonstrate the interaction between ABHD11‐AS1 and STAT3. RNA immunoprecipitation was subjected to prove the direct binding between ABHD11‐AS1 and EZH2. Immunofluorescence staining was performed to measure the expression and localization of TIMP2. EOC mouse model was conducted for validating the role of ABHD11‐AS1 in vivo. Results EGFR and ABHD11‐AS1 were highly expressed in EOC tissues and cell lines. Knockdown of EGFR or ABHD11‐AS1 inhibited cell growth, migration, and invasion of EOC cells. Expression of ABHD11‐AS1 was regulated by the activation of EGFR signaling pathway, mediated by STAT3. Besides, ABHD11‐AS1 was shown to silence TIMP2 by binding to chromatin‐modifying enzyme EZH2. Furthermore, inhibition of EGFR pathway or ABHD11‐AS1 repressed the tumor growth of EOC. Conclusion We defined the regulatory relationship between the EGFR signaling pathway, ABHD11‐AS1, EZH2, and TIMP2 suggesting that ABHD11‐AS1 may act as an oncogene and a potential target for antitumor therapies in ovarian cancer., EGFR and NEAT1 are upregulated in epithelial ovarian cancer. EGFR and NEAT1 promote proliferation, migration, and invasion of ovarian cancer cells. NEAT1 is upregulated by activation of EGFR signaling pathway.

Fang Xiao, Songshu Xiao, Min Xue Department of Obstetrics and Gynecology, Third Xiangya Hospital of Central South University, Changsha, Hunan 410013, People’s Republic of ChinaCorrespondence: Min XueDepartment of Obstetrics and Gynecology, Third Xiangya Hospital of Central South University, No. 138, Tongzipo Road, Yuelu District, Hexi, Changsha, Hunan 410013, People’s Republic of ChinaTel +86-13687354678Email xuemmm678@163.comBackground: Emerging proof suggests that microRNA (miRNA) malfunction is correlated to the generation and development of multiple malignancies. It has been proven that miRNA (miR)-139 represses a variety of malignancies. However, the understanding of its impact on ovarian cancer (OC) is insufficient. We aimed to investigate the expression and function of miR-139 in OC.Methods: The expression of mir-139 was detected and recorded, and the relationship of mir-139 remaining OC cells was explored. At the same time, we studied the correlation between ATP7A and mir-139 by the luciferase reporter test, Western blot, and quantitative real-time reverse transcription PCR.Results: The expression of miR-139 was remarkably downregulated in OC specimens. Furthermore, excessive miR-139 expression noticeably inhibited the migration, colony generation, proliferation, and invasion of OC cells. In addition, excessive miR-139 expression remarkably repressed the death and the expression of proteins related to cell death in OC cells, as well as inhibited the shedding of exosomes. According to the luciferase reporter test, Western blot, and quantitative real-time reverse transcription PCR, miR-139 directly targeted ATP7A. Furthermore, the expression of ATP7A was found to be negatively related to miR-139 levels in OC specimens. It was revealed via a rescue experiment that excessive ATP7A expression counteracted the repressive effect of miR-139 in OC cells.Conclusion: It was revealed via an in vivo study that miR-139 remarkably inhibited the growth of malignancies by downregulating ATP7A in nude mice. miR-139 represses the development of malignancies in OC by directly targeting ATP7A, offering an innovative approach for molecular therapy of OC.Keywords: apoptosis, ATP7A, exosome shedding, miR-139, ovarian cancer