Ovarian cancer (OC) is the gynecological malignancy type with the highest mortality rate in females. The regulatory effect of microRNAs (miRs) on their target genes serves a key role in tumor development. Therefore, in the present study, whether miR let-7d-5p targeting high mobility group A1 (HMGA1) regulated biological characteristics and chemosensitivity of OC cells by mediating the p53 signaling pathway was investigated. The let-7d-5p level was detected in OC tissues and adjacent normal tissues, followed by detection in OC cell lines SKOV3, A2780, OVCAR-3 and CaOV3, and human normal ovarian epithelial cell line (IOSE-80), in order to select the OC cell line for the following experiments. Subsequently, OC cells were treated with the let-7d-5p mimic, siHMGA1 and Tenovin-1. The targeting association between let-7d-5p and HMGA1 was then examined, and the OC cell viability, migration, cycle and apoptosis were evaluated. Subsequently, the chemosensitivity of OC cells to cisplatin was verified. Finally, expression levels of let-7d-5p, HMGA1, p21, B-cell lymphoma-2 (Bcl-2)-associated X (Bax), p27, p53 wild-type (p53 wt ), p53 mutated (p53 mut ), proliferating cell nuclear antigen (PCNA), cyclin-dependent kinase 2 (CDK2), matrix metallopeptidase (MMP)2, MMP9 and Bcl-2 were determined. As demonstrated in the results, let-7d-5p expression was low in OC tissues and had an increased reduction in the OVCAR-3 cell line. HMGA1 was confirmed as a target of let-7d-5p, and its expression was also silenced by let-7d-5p. let-7d-5p repressed OC cell viability, migration, cell cycle progression and apoptosis, while it promoted the chemosensitivity of OC cells to cisplatin by targeting HMGA1. The expression of let-7d-5p, p21, Bax, p27 and p53 wt was increased, while that of HMGA1, p53 mut , PCNA, CDK2, MMP2, MMP9 and Bcl-2 was reduced following cell transfection. The results in the present study provided evidence that let-7d-5p may suppress proliferation, and facilitate apoptosis and cisplatin chemosensitivity of OC cells by silencing HMGA1 via the p53 signaling pathway.

BackgroundEmerging evidences have demonstrated that lncRNAs play vital roles in various pathological processes, including cancer. The lncRNA WT1 antisense RNA (WT1-AS) serves as a tumor suppressor in various cancers. Nevertheless, the expression and precise function of WT1-AS in cervical carcinoma still remain not yet investigated. The objective of our study was to explore the expression of WT1-AS and its biological roles in cervical cancer.MethodsDifferences in the lncRNA expression profiles between cervical cancer and adjacent normal tissues were assessed by lncRNA expression microarray analysis. The expression of p53 in cervical cancer cell was assessed by qRT-PCR and immunofluorescence assay. Loss-of-function studies were used to explore the effect of lncRNA WT1-AS on the growth and metastasis of cervical cancer cell in vitro and in vivo.ResultsOur results demonstrated that WT1-AS was remarkably down-regulated in cervical carcinoma. Functional assays proved that up-regulation of WT1-AS significantly suppressed cervical cancer cell proliferation, migration and invasion. In addition, the luciferase reporter assay identified that miR-330-5p was the target of WT1-AS. Moreover, tumor suppressor p53 was identified as the direct target of miR-330-5p and alternation of miR-330-5p/p53 axis reversed the effects of WT1-AS in cervical cancer cell.ConclusionAltogether, our findings suggested that WT1-AS was down-regulated in cervical carcinoma and WT1-AS suppressed cervical carcinoma cell- proliferation, migration and invasion through regulating the miR-330-5p/p53 axis.

Annexin A2 is a member of the Annexin family that acts as a Ca2+-dependent phospholipid and membrane binding protein, which is associated with the survival and spread of multiple neoplasms. However, the function of Annexin A2 in ovarian cancer progression remains unclear. In this study, we aimed to investigate the role and underlying molecular mechanism of Annexin A2 in cell proliferation and invasion in ovarian cancer. We found that the mRNA expression of Annexin A2 was upregulated in ovarian cancer tissues and cell lines. In the loss-of-function of Annexin A2, β-catenin was indicated to be significantly suppressed and EMT constrained. Moreover, cell proliferation and invasion were both markedly inhibited by the downregulation of Annexin A2. Additionally, the overexpression of β-catenin obviously reversed the effect of Annexin A2 on EMT, and cell proliferation and invasion, indicating that Annexin A2 suppression regulated EMT through controlling β-catenin. Taken together, this study showed that Annexin A2 inhibition suppresses proliferation and invasion in ovarian cancer via β-catenin/EMT, proposing the potential role of Annexin A2 in the prevention and treatment of ovarian cancer.

Review question / Objective: (P) Population: Postmenopausal women with vaginal atrophy; (I) Intervention measures: oxytocin gel; (C) Control group: control group with only p l a c e b o g e l ; ( O ) R e s u l t : T h e t re a t m e n t e ff e c t o f postmenopausal women with vaginal atrophy. (S) Research type: Randomized controlled trials. Condition being studied: The dominant symptoms in the postmenopausal stage are urogenital system symptoms, previously described as vulvovaginal atrophy or atrophic vaginitis. As estrogen levels decrease in menopausal women, blood flow to the vagina and vulva also decreases, making these tissues thinner, drier, and less elastic, leading to impaired vaginal lubrication, burning, dryness, and atrophy. And an increase in pH value, which can affect sexual function and lead to difficulty in sexual intercourse. At present, estrogen is the gold standard for treatment, and low-dose vaginal hormone therapy is the foundation of treatment. However, some side effects may occur when estrogen is applied. At the same time, some studies have found that local application of oxytocin gel can alleviate vaginal atrophy and promote the proliferation of epithelial cells in the vagina. Therefore, oxytocin may serve as an alternative treatment for estrogen. INPLASY registration number: This protocol was registered with the International Platform of Registered Systematic Review and Meta-Analysis Protocols (INPLASY) on 01 June 2023 and was last u p d a t e d o n 0 1 J u n e 2 0 2 3 ( r e g i s t r a t i o n n u m b e r INPLASY202360006).