Abstract. Endometriosis is a prevalent and complex gynecological disease which affects 10% of women of reproductive age. Certain studies have suggested that a substantial number of microRNAs (miRNAs or miRs) are aberrantly or differentially expressed in the ectopic endometrium. To date, to the best of our knowlewdge, there is no report available on the role of miR-29 in the endometrium. In this study, we investigated the expression of the miR-29 family in the endometrium samples from women without endometriosis, as well as in paired ectopic and eutopic endometrium samples by reverse transcription-quantitative polymerase chain reaction (RT-qPCR). The results revealed that miR-29c was differentially expressed in the paired eutopic and ectopic endometrium samples. In addition, c-Jun was differentially expressed in the ectopic and eutopic endometrial tissues as determined by western blot analysis. Furthermore, the role of miR-29c in endometrial cell proliferation, invasion and apoptosis was examined in vitro. The results revealed that miR-29c exerted its effects on endometrial cells by suppressing cell proliferation and invasion, as well as promoting cell apoptosis. Furthermore, it was found that c-Jun was a novel target of miR-29c, and c-Jun reversed the effects of miR-29c on the proliferation, invasion and apoptosis of endometrial cells. To the best of our knowledge, this study is the first to identify miR-29c as a suppressor of endometriosis. Taken together, our results suggest that miR-29c exerts its effects on endometrial cell proliferation, apoptosis and invasion by inhibiting the expression of c-Jun. Our data may provide a novel potential therapeutic target for the treatment of endometriosis.

Pancreatic cancer (PC) is a lethal cancer in the digestive system. microRNAs (miRNAs) have been demonstrated to participate in PC progression. In this context, we thus aimed to explore the mechanism of miR-382 in epithelial mesenchymal transition (EMT) and lymph node metastasis in PC in relation to Anxa3 and the PI3K/Akt signaling pathway. Gene expression datasets GSE16515, GSE71989 and GSE32676 were screened out with the findings showed the significance of miR-382 and Anxa3 in PC. A total of 115 PC patients was selected for determination of miR-382 and Anxa3 expression with lowly expressed miR-382 and highly expressed Anxa3 found via RT-qPCR and western blot analysis. Additionally, negative correlation was found between miR-382 and Anxa3 in PC. Dual-luciferase reporter gene assay and in situ hybridization results confirmed that miR-382 negatively regulated Anxa3. miR-382 targeted Anxa3 and suppressed PC progression by blocking the PI3K/Akt signaling pathway. After a series of gain- and loss-of function approaches, up-regulation of miR-382 or silencing of Anxa3 inhibited the EMT and lymph node metastasis as evidenced by increased level of E-cadherin and decreased level of N-cadherin, Vimentin, VEGFR-3, VEGF-C and VEGF-D. Overexpression of miR-382 or downregulation of Anxa3 was shown to inhibit colony formation, migration and invasion abilities of PC cells. Further, tumor xenograft in nude mice in vivo also confirmed the inhibitory role of miR-382 and silenced Anxa3 in lymph node metastasis in PC. Thus, this study provides promising therapeutic targets for PC treatment.

Omega-3 fatty acids, especially eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), have been shown to possess definitively suppressive effects on the growth of epithelial ovarian cancer cells. This study investigated the differential effects of pure EPA and DHA on the growth of epithelial ovarian cancer cells and the potential molecular mechanisms that may be involved. There were significant time- and dose-dependent inhibitory effects of both EPA and DHA on cellular proliferation of the epithelial ovarian cancer cell line TOV-21G (P < 0.05). TOV-21G cells pretreated with peroxisome proliferator receptor activator gamma (PPARγ) antagonist, GW9662, markedly suppressed EPA/DHA-induced apoptosis as determined by TUNEL assay, Annexin V-FITC/PI staining, and caspase-3 activity. EPA/DHA significantly induced PPARγ and p53 overexpression as observed in immunoblotting assay and the induction of p53 by EPA/DHA was abolished by GW9662. In all cases, the effect of DHA was significantly more potent than that of EPA (P < 0.05). Our findings suggested that DHA may be more effective than EPA in growth suppression of TOV-21G cells and the biologic effects may be partly mediated by PPARγ and p53 activation. Further research is required to elucidate additional divergent mechanisms to account for apparent differences between EPA and DHA.

Objective. The use of cumulative live birth rate (CLBR) per ovarian stimulation cycle is proving to be an accurate method to calculate the success of IVF; however, the cycle outcome is closely associated with the number of embryos transferred (ET). Our aim was to report CLBR after IVF according to the number of embryos required to achieve a live birth in women aged ≥35 years, considering age, body mass index (BMI), and ethnicity. Methods. We conducted a retrospective cohort study including 1344 patients who underwent IVF between January 2013 and June 2016 at the First Affiliated Hospital of Xinjiang Medical University. The cumulative probability of live birth for each couple was estimated using the Kaplan–Meier method, and survival curves were compared according to age, BMI, and ethnicity using the log-rank test. Results. CLBR increased rapidly from 1 to 5 ETs, moderately from 6 to 10 ETs, and slowly thereafter. CLBR was significantly different across 4 categories based on BMI as well as across those based on age; low CLBR was significantly associated with the age of ≥42 years and obesity. Conclusion. The association between CLBR and number of ET provides realistic and precise information regarding the success of IVF and can be applied to guide clinicians and patients.

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Herein, we used DIANA TOOLS, GEPIA and other bioinformatics databases to predict regulatory pathways in breast cancer. Accordingly, we clarified the regulatory mechanism of EYA2 on miR-93 expression to aggravate breast cancer, which was involved with the STING signaling pathway. CCK-8 assay, scratch test, Transwell assay, and flow cytometry were applied to detect cell viability, migration, invasion, and apoptosis. The experimental data found that EYA2 was highly expressed in breast cancer tissues and cells and associated with poor prognosis. Overexpression of miR-93 in breast cancer was positively correlated with EYA2. EYA2 promoted miR-93 expression, advanced breast cancer cell proliferation and inhibited their apoptosis. Results of luciferase assay showed that miR-93 was enriched in the STING 3'UTR. Furthermore, knockdown of EYA2 inhibited the expression of miR-93, promoted the expression of STING, and inhibited the tumor growth. In response to EYA2 knockdown, the expression of IFN-β and ISG was increased, and PD-L1 was decreased. In addition, the phosphorylation level of TBK1 and IRF3 was enhanced, the percentage of myeloid-derived suppressor cells in blood was reduced, and secretion of IFN-β and IL-12 was enhanced. In conclusion, EYA2 upregulates miR-93 expression and promotes malignancy of breast cancer by targeting and inhibiting the STING signaling pathway.

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