MicroRNA-23a depletion promotes apoptosis of ovarian cancer stem cell and inhibits cell migration by targeting DLG2.

Ovarian cancer (OC) is xenogeneic that is influenced by many generated factors related to epigenetic factors to accelerate tumor metastasis. This study was conducted with the objective of investigating the effect of microRNA-23a-3p (miR-23a) on the biological characteristics of OC stem cells by targeting discs large homolog 2 (DLG2). OC-related differentially expressed genes were screened by microarray-based gene expression analysis, after which a list of miRNAs that regulate the genes was predicted. In total, 50 patients diagnosed with OC were enrolled in this study. DLG2 positive protein expression was measured in OC tissues. The interaction between DLG2 and miR-23a was predicted and analyzed through luciferase activity measurement. With the intervention of miR-23a and/or DLG2 expression in OC stem cells, the expression of miR-23a, DLG2, Bax, Bcl-2, Oct-4, and Nanog was determined. Afterward, different cell experiments were conducted to examine the regulation effect of miR-23a in OC stem cells. Tumor formation in vivo was also evaluated in nude mice. DLG2 had low expression in OC. The results showed that there was a decrease in the expression of Bcl-2, Oct-4, and Nanog, while DLG2 and Bax were increased as a result of miR-23a depletion. In addition, when miR-23a was suppressed, cell viability, migration, invasion, cloning, and renewal abilities of OC stem cells were decreased, while apoptosis ability was enhanced. As a target gene of miR-23a, DLG2 downregulation reversed the suppressive function of miR-23a in the inhibition of OC development. Finally, in vivo experiment verified that miR-23a downregulation restrained the tumor growth in OC stem cells. In conclusion, our findings suggested that the inhibition of miR-23a results in the suppression of OC progression by releasing DLG2, which provides new understanding on the potential therapeutic effect of miR-23a inhibition in OC patients.

Silencing CCAT2 inhibited proliferation and invasion of epithelial ovarian carcinoma cells by regulating Wnt signaling pathway.

Long non-coding RNA CCAT2 (colon cancer-associated transcript 2) is dysregulated in varieties of human tumors. However, the role of CCAT2 in epithelial ovarian carcinoma (EOC) is not yet known clearly. The aim of this study is to investigate the effects of CCAT2 on proliferation and invasion of EOC cells and the potential mechanisms by which CCAT2 functions. In the present paper, we found that knockdown of CCAT2 impaired cell proliferation and invasion in vitro. Furthermore, we also studied the role of CCAT2 in the modulation of Wnt/ß-catenin signaling pathway. Our results showed that knockdown of CCAT2 inhibited the expression of ß-catenin and the activity of TCF/LEF (T-cell factor/lymphoid enhancer factor) acting as a key transcription factor of Wnt/ß-catenin signaling pathway. In addition, we found that silencing CCAT2 down-regulated the expression of c-MYC and MMP-7. But, that was reversed by the treatment with LiCl (lithium chloride) which could activate canonical Wnt/ß-catenin signaling pathway. Taken together, these results indicate that CCAT2 may promote ovarian cancer progression, at least partly, through Wnt/ß-catenin signaling pathway. Thus, CCAT2 might represent a novel therapeutic target for ovarian cancer.

[Study on the status and related socio-psychological factors of maternal depression among high-risk pregnancy women in Harbin city].

OBJECTIVE: This study aimed to investigate the depression status among high-risk pregnancy women, and to analyze its relevant social and psychological factors. METHODS: A total of 42 high-risk pregnancy women and 40 normal pregnancy women in a teaching hospital in Harbin city were followed up at time points of 32 - 36 weeks pregnancy, one week before labor, one week postpartum, and six weeks postpartum, respectively. During follow-up, the basic situation, social psychosocial factors of pregnancy women were collected and the depression of pregnancy women was measured by self-designed questionnaire and self-rating depression scale. The Edinburgh Postnatal Depression Scale (EPDS) was applied at timepoint of one week postpartum. Single factor analysis and the unconditional multivariate logistic regression were applied for analyzing the on the related social-psychosocial factors among high-risk pregnancy women. RESULTS: The age of high-risk pregnancy women was (31.0±5.6), and the age of normal pregnancy women was (30.5±3.8) (t=0.169, P>0.05). The results showed that the depression rate in high-risk pregnancy women was 45.2% (19/42), which was 25.0% (10/40) in normal pregnancy women, the difference was significant (χ2=3.671, P=0.045). The depression rates at different time points were 30.9% (13/42), 42.9% (18/42), 23.8% (10/42), 26.2% (11/42) in high-risk pregnancy women respectively, and 25.0% (10/40), 15.0% (6/40), 20.0% (8/40), 17.5% (7/40) in the control group respectively, the difference of the depression rates among groups at one week before labor was significant (χ2=7.680, P<0.01), the difference among groups at 32-36 weeks pregnancy (χ2=0.133, P=0.80), at one week postpartum (χ2=0.174, P=0.79) and at six weeks postpartum (χ2=0.903, P=0.43) were not significant. At one week postpartum and six weeks postpartum periods, the EPDS depression rate were 12.5% (4/32), 30.4% (7/23) in case group respectively, 8.3% (3/36), 22.9% (8/35) in control group respectively, the difference were not significant (χ2=0.319, 0.416, P=0.573, 0.519). There were significantly associations between the depression mood of one week before labor and the depressive symptoms of six weeks postpartum in both groups (r=0.824, 0.677, both P values were <0.05). The risk factors for maternal depression among high-risk pregnancy women were not ready for production (OR=2.73, P<0.01) and fearing of childbirth safety (OR=2.89, P<0.01). CONCLUSION: The depression date of high-risk pregnancy was high, especially at the time point one week before labor. Risk factors of maternal depression among high-risk pregnancy were "not ready for production" and "fear of childbirth safety".

[Effects of DCC gene on cell growth and chemosensitivity of ovarian epithelial carcinoma cells].

OBJECTIVE: To study the effects of DCC gene transfection on cell-growth and chemosensitivity of ovarian epithelial carcinoma cell line HO8910. METHODS: Recombinant eukaryotic expression vector pcDNA3.1(+)-DCC containing DCC gene was introduced by lipofectamine transfection reagent into ovarian epithelial carcinoma cell line HO8910 which does not express DCC endogenously. The expression of DCC was detected by RT-PCR and immunocytochemistry. The cell proliferation and the viability rate after different concentrations of cisplatin and paclitaxel were given were assessed by methyl thiazolyl tetrazolium (MTT) assay. RESULTS: Exogenous DCC gene had been successfully transferred into HO8910 cells and obtained permanent expression. The growth speed of HO8910-DCC cells was significantly slower than other two groups. There was a significant difference between them (P < 0.01) except at the first day after being planted. There was no difference between the growth speed of HO8910 cells and that of HO8910-Neo cells (P > 0.05). The viability rate of HO8910-DCC cells was significantly lower than other two groups after (0.1 - 5.0) peak plasma concentration (PPC) of cisplatin and paclitaxel were given (P < 0.01). The viability rate of HO8910-DCC cells was lower than other two groups after 10.0 PPC concentration of cisplatin was given (P < 0.05), but there was no difference between them after 10.0 PPC concentration of paclitaxel was given (P > 0.05). The viability rate of HO8910 cells was similar to HO8910-Neo cells after different concentrations of cisplatin and paclitaxel were given (P > 0.05). CONCLUSION: The DCC gene expression not only inhibits cell growth but also enhances the chemosensitity of ovarian epithelial carcinoma cell line HO8910.