AIM:To investigate the role of BRCA2 and CDKN1A interacting protein(BCCIP)in gastric can-cer(GC)and elucidate its mechanism in mediating cisplatin resistance.METHODS:The BCCIP mRNA expression was assessed in GC tissues(n=415)and normal tissues(n=34)using The Cancer Genome Atlas(TCGA)database.In an in-ternal cohort(n=36 for RT-qPCR;n=5 for Western blot;n=30 for immunohistochemistry),BCCIP expression at both mRNA and protein levels was examined in GC tissues and paired adjacent normal tissues.Human GC cell lines AGS and HGC27 were cultured in vitro and treated with cisplatin in a dose(0,2,4,6,8 and 10 μmol/L)-and time(0,6,24 and 48 h)-dependent manner,followed by Western blot analysis of BCCIP expression.Stable BCCIP knockdown cell lines(shRNA#1 and shRNA#2 groups)were generated via lentiviral transfection,with empty vector-transfected cells serving as controls(vector group).Flow cytometry and colony formation assay were performed to evaluate the effects of BCCIP on apoptosis and colony-forming ability of GC cells treated with cisplatin.Western blot was utilized to detect the changes of BCCIP protein expression levels in the cytoplasm and nucleus of GC cells after cisplatin(2.5 and 1.0 μmol/L)treatment,as well as the effects of BCCIP on the expression of DNA damage marker γ-H2AX and apoptosis-related proteins cleaved caspase-9 and cleaved caspase-3,and the activation of checkpoint kinase 1(CHK1)after cisplatin(2.5 and 1.0 μmol/L)treatment.Immunofluorescence was conducted to observe the effect of BCCIP on γ-H2AX expression in GC cells treated with cisplatin(2.5 and 1.0 μmol/L).RESULTS:The BCCIP expression was significantly up-regulated in GC tissues compared with normal tissues(P<0.01).Cisplatin induced up-regulation of BCCIP expression in a dose-and time-depen-dent manner.Knockdown of BCCIP significantly enhanced cisplatin-induced apoptosis(P<0.01)and reduced colony-forming ability(P<0.05)of GC cells.Knockdown of BCCIP promoted the expression of γ-H2AX,but inhibited the activa-tion of CHK1 after cisplatin treatment,with increased protein levels of cleaved caspase-9 and cleaved caspase-3(P<0.01).CONCLUSION:Cisplatin promotes the expression of BCCIP in GC cells.BCCIP confers cisplatin resistance in GC cells by suppressing apoptosis through modulation of DNA damage response pathways.

AIM:To investigate the role of BRCA2 and CDKN1A interacting protein(BCCIP)in gastric can-cer(GC)and elucidate its mechanism in mediating cisplatin resistance.METHODS:The BCCIP mRNA expression was assessed in GC tissues(n=415)and normal tissues(n=34)using The Cancer Genome Atlas(TCGA)database.In an in-ternal cohort(n=36 for RT-qPCR;n=5 for Western blot;n=30 for immunohistochemistry),BCCIP expression at both mRNA and protein levels was examined in GC tissues and paired adjacent normal tissues.Human GC cell lines AGS and HGC27 were cultured in vitro and treated with cisplatin in a dose(0,2,4,6,8 and 10 μmol/L)-and time(0,6,24 and 48 h)-dependent manner,followed by Western blot analysis of BCCIP expression.Stable BCCIP knockdown cell lines(shRNA#1 and shRNA#2 groups)were generated via lentiviral transfection,with empty vector-transfected cells serving as controls(vector group).Flow cytometry and colony formation assay were performed to evaluate the effects of BCCIP on apoptosis and colony-forming ability of GC cells treated with cisplatin.Western blot was utilized to detect the changes of BCCIP protein expression levels in the cytoplasm and nucleus of GC cells after cisplatin(2.5 and 1.0 μmol/L)treatment,as well as the effects of BCCIP on the expression of DNA damage marker γ-H2AX and apoptosis-related proteins cleaved caspase-9 and cleaved caspase-3,and the activation of checkpoint kinase 1(CHK1)after cisplatin(2.5 and 1.0 μmol/L)treatment.Immunofluorescence was conducted to observe the effect of BCCIP on γ-H2AX expression in GC cells treated with cisplatin(2.5 and 1.0 μmol/L).RESULTS:The BCCIP expression was significantly up-regulated in GC tissues compared with normal tissues(P<0.01).Cisplatin induced up-regulation of BCCIP expression in a dose-and time-depen-dent manner.Knockdown of BCCIP significantly enhanced cisplatin-induced apoptosis(P<0.01)and reduced colony-forming ability(P<0.05)of GC cells.Knockdown of BCCIP promoted the expression of γ-H2AX,but inhibited the activa-tion of CHK1 after cisplatin treatment,with increased protein levels of cleaved caspase-9 and cleaved caspase-3(P<0.01).CONCLUSION:Cisplatin promotes the expression of BCCIP in GC cells.BCCIP confers cisplatin resistance in GC cells by suppressing apoptosis through modulation of DNA damage response pathways.

Purpose: The current meta-analysis combining mid and low rectal cancer with no meta-analysis only for low rectal cancer was seen. This meta-analysis was to compare the short- and mid-term outcomes of the transanal total mesorectal excision (TaTME) vs. laparoscopic total mesorectal excision (LaTME) for low rectal cancer. Methods: A systematic literature search was conducted using the web-based databases; China National Knowledge Infrastructure, Chinese BioMedical Database, PubMed, Embase, Cochrane Central Register of Controlled Trials, and Wanfang Database. Randomized controlled trials (RCTs) were evaluated using the Jadad scale and non-RCTs (NRCs) were evaluated using the Newcastle-Ottawa Scale. Results: Ten studies (2 RCTs and 8 NRCs) involving 772 patients were included. Among them, 378 patients underwent TaTME and 394 patients underwent LaTME. Compared with the LaTME group, the conversion rate was low (risk ratio [RR], 0.25; 95% confidence interval [CI], 0.11–0.54; P < 0.001), the circumferential resection margin (CRM) involvement was low (RR, 0.48; 95% CI, 0.27–0.86; P = 0.010), and the hospital stay was short (mean difference, –1.72; 95% CI, –2.89 to –0.55; P = 0.004) in the TaTME group. No significant differences were seen in the mesorectal resection quality, CRM distance, distal resection margin (DRM) involvement, DRM distance, local R1 resection, intraoperative complications, morbidity, anastomotic leakage, severe morbidity, mortality, operative time, intraoperative blood loss, harvested lymph nodes, and local recurrence rate (P > 0.05). Conclusion The TaTME is a promising surgical technique and is fully a safe and efficacious option in managing low rectal cancer.

Objective To know the current situation of core competency of midwives in Guangzhou, and analyze the influencing factors.Methods A cross sectional survey was conducted among 256 midwives from 13 hospitals in Guangzhou to investigate their core competency.Results The total average score of core competency of midwives was (4.09±0.49). The scores of intrapartum care and antenatal care were higher,while the scores of progestational care and public health care were lower. Multivariate regression analysis showed that the core competency of midwives was influenced by several aspects,and they were work experience,work experience in midwifery,age,title,job and marital status (β′=0.771, 0.549,0.409,0.390,0.250,0.137;P<0.05).Conclusions The overall level of midwifery competency of midwives in Guangzhou is good,but their professional scope and role function need to be deepen and expanded,so as to satisfy the growing health care demand from pregnant women and their families. Managers should develop individualized and specific training and management strategies to improve midwives′ competency based on the condition of hospitals.