Effect of laparoscopic-assisted transvaginal hysterectomy on wound complications in patients with early stage cervical cancer: A meta-analysis.

Laparoscopic-assisted vaginal radical hysterectomy (LARVH) and abdominal radical hysterectomy (ARH) have been widely applied to treat cervical carcinoma. But LARVH and ARH have not been fully investigated in treating cervical carcinoma after injury associated with injury. This research is intended to provide an up-to-date basis for comparing LARVH with ARH in early stage cervical carcinoma. Comparison between LARVH and ARH in cervical carcinoma was carried out through a combination of related research. Eligible articles from databases such as PubMed and Embase were screened using an established search strategy. This report covered the results of LARVH versus ARH in cervical carcinoma. The average difference and the 95% confidence interval (CI) were used for the combination of consecutive variables. The combination of categorical variables was performed with the odds ratio (OR) 95% confidence interval. Through the identification of 1137 publications, eight of them were chosen to be analysed. Among them, 363 were treated with LARVH and 326 were treated with ARH. Eight trials showed that LARVH was associated with a reduced risk of postoperative wound infection than ARH (OR, 0.23; 95% CI, 0.1-0.55, p = 0.0009). Five trials showed that there was no difference in the risk of postoperative bleeding after surgery (OR, 1.17; 95% CI, 0.42-3.29, p = 0.76). We also did not differ significantly in the duration of the surgery (OR, 1.79; 95% CI, -6.58 to 10.15, p = 0.68). So, the two surgical methods differ significantly only in the risk of postoperative wound infection.

TAZ Regulates the Cisplatin Resistance of Epithelial Ovarian Cancer Cells via the ANGPTL4/SOX2 Axis.

Objective: Epithelial ovarian cancer (EOC) is a fatal gynecological malignancy. This study explored the mechanism of TAZ in regulating drug sensitivity of cisplatin (DDP-)-resistant EOC cells through the ANGPTL4/SOX2 axis. Methods: The A2780/DDP cells were prepared by stepwise progressive concentration method. The drug resistance and TAZ expression in EOC cells were determined. Drug sensitivity was measured after TAZ overexpression in A2780 cells and TAZ downregulation in A2780/DDP cells, respectively. The effects of TAZ knockdown on apoptosis rate, stemness, and cancer stem cell (CSC) marker (CD44, OCT4, and ALDH1A) levels in A2780/DDP and DDP-treated A2780/DDP cells were assessed. The binding of TAZ and ANGPTL4 was verified using ChIP-qPCR, and ANGPTL4 and SOX2 levels were determined. The effects of different combined treatments of TAZ, ANGPTL4, and SOX2 on drug sensitivity of A2780/DDP cells and DDP-treated A2780/DDP cells were evaluated. Results: TAZ was upregulated in drug-resistant EOC cells. TAZ knockdown significantly increased the drug sensitivity of A2780/DDP cells, while TAZ overexpression markedly decreased the drug sensitivity of A2780 cells. TAZ silencing promoted apoptosis of drug-resistant EOC cells and inhibited cell stemness. TAZ targeted ANGPTL4 and TAZ silencing enhanced drug sensitivity of A2780/DDP cells by inhibiting ANGPTL4. ANGPTL4 overexpression elevated SOX2 expression, and SOX2 downregulation reduced the drug resistance and promoted the apoptosis of A2780/DDP cells. Conclusion: TAZ regulates DDP sensitivity of drug-resistant EOC cells via the ANGPTL4/SOX2 axis.

Long noncoding RNA SNHG3 promotes malignant phenotypes in cervical cancer cells via association with YAP1.

Long non-coding RNA (LncRNA) Small Nucleolar RNA Host Gene 3 (SNHG3) is involved in the occurrence and development of various cancers. However, the exact function and mechanism of SNHG3 in cervical cancer (CC) are still unclear. In this context, we identified a significant increase of SNHG3 expression in CC tissues. Upregulation of SNHG3 expression was associated with advanced FIGO stage and metastasis, and indicated poor overall survival of the CC patients. Functionally, SNHG3 enhanced the proliferation, migration and invasion of CC cells in vitro, and facilitated CC growth in vivo. Further investigation uncovered that SNHG3 interacted with oncoprotein YAP1, thus suppressing its degradation. Additionally, SNHG3 modulated the transcription of several target genes of YAP1. The oncogenic role of SNHG3 was partially attributable to YAP1. Taken together, our research revealed the prognostic and functional roles for SNHG3 in CC, suggesting that SNHG3 could serve as a biomarker for prognosis and a therapeutic target for CC.

Microarray data analysis reveals gene expression changes in response to ionizing radiation in MCF7 human breast cancer cells.

BACKGROUND: The aim of this study was to identify potential therapeutic target genes for breast cancer (BC) by the investigation of gene expression changes after ionizing radiation (IR) in BC cells. Gene expression profile GSE21748, including BC cell line MCF-7 samples at different time points after IR treatment, were downloaded from Gene Expression Omnibus. Differentially expressed genes (DEGs) were identified in different time points following IR compared with cell samples before IR, respectively. Gene ontology functions and The Kyoto Encyclopedia of Genes and Genomes pathways of the overlapping DEGs were enriched using DAVID. Transcription factor (TFs)-encoding genes were identified from the overlapping DEGs, followed by construction of transcriptional regulatory network and co-expression network. RESULTS: A total of 864 overlapping DEGs were identified, which were significantly enriched in regulation of cell proliferation and apoptosis, and cell cycle process. We found that FOXD1, STAT6, XBP1, STAT2, LMO2, TFAP4, STAT3, STAT1 were hub nodes in the transcriptional regulatory network of the overlapping DEGs. The co-expression network of target genes regulated by STAT3, STAT1, STAT6 and STAT2 included some key genes such as BCL2L1. CONCLUSION: STAT1, STAT2, STAT3, STAT6, XBP1, BCL2L1, CYB5D2, ESCO2, and PARP2 were significantly affected by IR and they may be used as therapeutic gene targets in the treatment of BC.

Intramuscular versus intravenous oxytocin for the third stage of labor after vaginal delivery to prevent postpartum hemorrhage: a meta-analysis of randomized controlled trials.

INTRODUCTION: To examine the effects and safety of oxytocin administered intramuscularly or intravenously for preventing postpartum hemorrhage (PPH) in the third stage of labor after vaginal deliveries. MATERIAL AND METHODS: Before data extraction, the review was registered with the PROSPERO International Prospective Register of Systematic Reviews (registration No. CRD42019145912). We searched the published electronic databases, including Medline, EMBASE, PubMed, Web of Science, CNKI, VIP, Wanfang, the Cochrane Library, clinicaltrial.gov and PROSPERO database, from their inception until February 2019. We included all randomized controlled trials (RCTs) comparing intramuscular and intravenous oxytocin administered just after the birth of the anterior shoulder or soon after the birth of the baby during a vaginal delivery. The primary outcomes were the incidence of PPH and severe PPH. PPH was defined as a blood loss ≥500 ml within 24 hours after vaginal birth. Severe PPH refers to a clinically estimated blood loss equal to or greater than 1000 mL within 24 hours after vaginal birth. Statistical heterogeneity was assessed by the I2 test, the Cochran Q statistic and the Galbraith plot for heterogeneity. RESULTS: Six RCTs, including 7320 women undergoing vaginal delivery, were identified in the meta-analysis. Women who were randomized to have intravenous oxytocin for the third stage of labor had a significantly lower incidence of PPH (relative risk 1.35, 95% CI 1.11-1.64, p = 0.003), severe PPH (relative risk 1.61, 95% CI 1.05-2.46, p = 0.03) and blood transfusion (relative risk 2.50, 95% CI 1.37-4.59, p = 0.003) compared with those who were randomized to have intramuscular oxytocin during the third stage of labor after vaginal delivery. There was no significant difference with regard to changes in hemoglobin level, third stage of labor duration, mean postpartum blood loss, or the incidences of a need for additional uterotonics and of retained placenta or manual removal of placenta between groups. CONCLUSIONS: For women in the third stage of labor who are undergoing a vaginal delivery, the use of intravenous oxytocin reduces the incidence of PPH, severe PPH and blood transfusion and does not increase the risk of adverse effects compared with intramuscular oxytocin.

[Involvement of miR-199a in cisplatin resistance of ovarian cancer cell through modulating expression of mTOR].

OBJECTIVE: To study the effect of miR-199a on the sensitivity of OV2008 and C13* cells to cisplatin and investigate its mechanism of action. METHODS: Real-time polymerase chain reaction(PCR) and Western blot were applied to detect the expression level changes of mammalian target of rapamycin (mTOR) in OV2008 and C13* cells before and after transfecting the cells with the mimics and inhibitor of miR-199a with Lipofectamine 2000.We constructed luciferase reporter vectors of mTOR and then transfected OV2008 cells with the mimics of miR-199a with Lipofectamine 2000 to study the regulation of miR-199a's downstream target genes. RESULTS: The expression level of mTOR was significantly higher in C13* than OV2008 cells (P<0.05). After OV2008 and C13* cells were transfected with the mimics and inhibitor of miR-199a, real-time PCR and Western blot showed that the mimics of miR-199a repressed the expression of mTOR; and the inhibitor of miR-199a promoted the expression of mTOR. After transfecting OV2008 cells with the mimics of miR-199a and luciferase reporter vectors of mTOR, renillaluciferase reporter gene analysis indicated the expression level of mTOR was negatively regulated by miR-199a. CONCLUSION: miR-199a regulates the sensitivity of ovarian cancer cells to cisplatin through modulating expression of mTOR, and involves in the cisplatin resistance process of ovarian cancer cells.