BackgroundPrevious studies have suggested that metformin may be useful for preventing and treating endometrial cancer (EC), while the results have been inconsistent. This systematic review and meta-analysis aimed to investigate the association between metformin use and risk and prognosis of patients with EC.MethodsPubMed, Embase, and the Cochrane Library databases were searched for observational studies evaluating the effect of metformin on EC prevention or treatment. The odds ratio (OR) was used for analyzing risks, and the hazard ratio (HR) was used for analyzing survival outcomes. A random-effects model was used for data analysis.ResultsSeven studies reported data on EC risk. The pooled results suggested that metformin was not significantly associated with a lower risk of EC [OR = 1.05, 95% confidence interval (CI) 0.82–1.35, P = 0.70]. For patients with diabetes, metformin showed no advantage in reducing the EC risk compared with other interventions (OR = 0.99, 95% CI 0.78–1.26, P = 0.95). Further, seven studies were included for survival analysis. The pooled data showed that metformin could significantly improve the overall survival of patients with EC (HR = 0.61, 95% CI 0.48–0.77, P < 0.05) and reduce the risk of EC recurrence (OR = 0.50, 95% CI 0.28–0.92, P < 0.05) Finally, we noted metformin was associated with significantly improving the overall survival of EC patients among diabetes (HR = 0.47; 95%CI 0.33–0.67, P < 0.05).ConclusionsThis meta-analysis did not prove that metformin was beneficial for preventing EC. However, metformin could prolong the overall survival of patients with EC and reduce their risk of cancer relapse.Electronic supplementary materialThe online version of this article (10.1186/s12885-018-4334-5) contains supplementary material, which is available to authorized users.

Cervical cancer (CC) remains one of the leading malignancies afflicting females worldwide, with its aetiology associated with long‐term papillomavirus infection. Recent studies have shifted their focus and research attention to the relationship between long non‐coding RNAs (lncRNAs) and CC therapeutic. Thus, the aim of the current study was to investigate the underlying mechanism of lncRNA LINC01305 on the cell invasion, migration and epithelial‐mesenchymal transition (EMT) of CC cells via modulation of the PI3K/Akt signalling pathway by targeting tenascin‐X B (TNXB). The expressions of LINC01305, TNXB, MMP2, MMP9, E‐cadherin, vimentin, PI3K, Akt, p‐PI3K, p‐Akt and TNXB were detected in this study. After which, the cell invasion and migration abilities of the CC cells were determined respectively. Bioinformatics and the application of a dual luciferase reporter gene assay provided verification indicating that TNXB is the target gene of lncRNA LINC01305. Reverse transcription quantitative polymerase chain reaction (RT‐qPCR) and western blot analysis methods revealed that the expressions of MMP2, MMP9, vimentin, PI3K, Akt, p‐PI3K and p‐Akt were decreased following the down‐regulation of LncRNA LINC01305 or overexpression of TNXB. LncRNA LINC01305 silencing or TNXB overexpression was noted to decrease the migration and invasion of SiHa cells. Taken together, the key findings of the current study present evidence suggesting that lncRNA LINC01305 silencing suppresses EMT, invasion and migration via repressing the PI3K/Akt signalling pathway by means of targeting TNXB in CC cells, which ultimately provides novel insight and identification of potential therapeutic targets for CC.

Long non-coding RNAs (lncRNAs) play critical roles in the initiation and progression of human cancers. HOX transcript antisense RNA (HOTAIR) is an lncRNA localized to the mammalian HOXC gene cluster; it can interact with polycomb repressive complex 2 and the lysine-specific histone demethylase/CoREST/REST complex, and it manipulates the expression of various genes. HOTAIR promotes tumor invasion and metastasis by silencing tumor suppressors, and activating oncogenes and signaling pathways. HOTAIR is deregulated in many human cancers; despite its critical roles in health and disease, the underlying mechanisms governing HOTAIR function are unknown. In this review, we summarize the recent findings on the roles of HOTAIR in gynecologic cancers.

BackgroundMicroRNA-365 (miR-365) has been reported to be a tumor suppressor miRNA. However, the role of miR-365 in progression of endometrial cancer (EC) has not been explored, in this study, we have found that re-expression of miRNA-365 inhibits cell proliferation, causes apoptosis and senescence.Materials and methodsOverexpression of miR-365 attenuated cell migration and invasion, inhibited sphere-forming capacity, and enhanced the chemosensitivity to paclitaxel. In silico prediction tools identified the potential targets of miR-365.ResultsWe identified EZH2 and FOS as targets of miR-365 and found that downregulating these genes imitated the tumor suppressive effect of miR-365. The outcomes of the study suggested that a reverse correlation existed between low miR-365 and overexpression of FOS and EZH2 in EC tissue specimens.ConclusionThe study concludes that miR-365 acts as an important tumor suppressor and contributes by suppressing cell invasiveness, proliferation, and self-renewal in cancer cell lines by regulating multiple oncogenes. We establish that miR-365-EZH2/FOS pathway is an important target for treating EC.

Cervical cancer (CC) remains a distinct public health stumbling block worldwide. Increasing evidence has highlighted long non-coding RNAs (lncRNAs) as tumor-associated biological molecules. In this study, by means of altering the expression of lncRNA RP1-93H18.6 in CC cells, its ability to influence the biological activities of CC cells was evaluated. Differentially expressed lncRNAs were initially screened from the GEO database. A series of RP1-93H18.6 vectors, small interfering RNA (siRNA) against RP1-93H18.6, and LY294002 (an inhibitor for the phosphatidylinositol 3-kinase [PI3K]/Akt [serine/threonine kinase] axis) were introduced in a respective manner to treat the HeLa cells in order to analyze their effects on cellular activities in vitro. Nude mice with xenograft tumors were utilized in order to assess CC tumor growth and metastasis in vivo. lncRNA RP1-93H18.6 was highly expressed in CC, which could activate the P13K/Akt axis. RP1-93H18.6 vectors exposure increased cell viability, adhesion, migration, and invasion, which resulted in more cells arrested at the S stage and reduced apoptosis, while acting to promote tumor growth and metastasis. The siRNA against RP1-93H18.6 or LY294002 exposure was observed to attenuate the effects induced by RP1-93H18.6 vectors. This study suggests that suppression of lncRNA RP1-93H18.6 exerts potent inhibitory effects on the development and progression of CC via blockade of the PI3K/Akt axis.