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Xiao Tang,Kun Tong,Lishan Zhu,Guoqing Fu,Wei Chang,Ting Zhou,Zhibing Zhang,Ling Tong,Ling Zhang,Yuqin Shi,Ling Zhang,Yuqin Shi 대한독성 유전단백체 학회 2016 Molecular & cellular toxicology Vol.12 No.4
Di-2-ethylhexyl phthalate (DEHP) which belongs to phthalatic-acid esters, is a kind of harmful, global environmental pollutants. It is a known endocrine disrupting chemical and male reproductive toxicant. However, the mechanism by which DEHP exposure result in male reproductive toxicity is still unclear. To elucidate the productive toxicity mechanism of DEHP, we attemptted to investigate oxidative stress, apoptotic effects, mRNA and protein expression of apoptosis-associated genes including FasL, caspase-3, and caspase-8 in GC-2spd (mouse spermatogenic cells). The results showed that, with the increase of DEHP concentration, cell apoptosis rate increased; the activities of relation index of oxidative stress such as malondialdehyde (MDA), superoxide dismutase (SOD) and glutatione peroxidase (GSH-PX) changed significantly; the mRNA and protein expression levels of FasL, caspase-3, -8, altered obviously. These results suggested that DEHP could induce apoptosis of GC-2spd cells through oxidative stress and FasL-dependent pathway.
Luo, Ting,Chen, Long,He, Ping,Hu, Qian-Cheng,Zhong, Xiao-Rong,Sun, Yu,Yang, Yuan-Fu,Tian, Ting-Lun,Zheng, Hong Asian Pacific Journal of Cancer Prevention 2013 Asian Pacific journal of cancer prevention Vol.14 No.4
Vascular endothelial growth factor (VEGF) is a potent regulator of angiogenesis and thereby involved in the development and progression of solid tumours. Associations between three VEGF gene polymorphisms (-634 G/C, +936 C/T, and +1612 G/A) and breast cancer risk have been extensively studied, but the currently available results are inconclusive. Our aim was to investigate associations between three VEGF gene polymorphisms and breast cancer risk in Chinese Han patients. We performed a hospital-based case-control study including 680 female incident breast cancer patients and 680 female age-matched healthy control subjects. Polymerase chain reaction restriction fragment length polymorphism (PCR-RFLP) analysis was performed to detect the three VEGF gene polymorphisms. We observed that women carriers of +936 TT genotypes [odds ratio (OR) =0.46, 95% confidence interval (CI) = 0.28, 0.76; P=0.002] or 936 T-allele (OR=0.81, 95% CI= 0.68, 0.98; P=0.03) had a protective effect concerning the disease. Our study suggested that the +1612G/A polymorphism was unlikely to be associated with breast cancer risk. The -634CC genotype was significantly associated with high tumor aggressiveness [large tumor size (OR=2.63, 95% CI=1.15, 6.02; P=0.02) and high histologic grade (OR=1.47, 95% CI= 1.06, 2.03; P=0.02)]. The genotypes were not related with other tumor characteristics such as regional or distant metastasis, stage at diagnosis, or estrogen or progesterone receptor status. Our study revealed that the VEGF -634 G/C and +936 C/T gene polymorphisms may be associated with breast cancer in Chinese Han patients.
Liu, Yi-Ting,Shi, Jing-Pu,Fu, Ling-Yu,Zhou, Bo,Wang, Hai-Long,Wu, Xiao-Mei Asian Pacific Journal of Cancer Prevention 2013 Asian Pacific journal of cancer prevention Vol.14 No.1
Many epidemiological studies in Asian populations have investigated associations between the Arg399Gln gene polymorphism of X-ray repair cross complementing gene 1 (XRCC1) and risk of cervical carcinoma, but no conclusions have been available because of controversial results. Therefore a meta-analysis was conducted for clarification. Relevant studies were identified by searching the Pubmed, Embase, the Web of Science, Cochrane Collaboration's database, Chinese National Knowledge Infrastructure (CNKI), Wanfang database and China Biological Medicinse (CBM) until September, 2012. A total of eight studies were included in the present meta-analysis, which described 1,759 cervical carcinoma cases and 2,497 controls. Odds ratios (ORs) and corresponding 95% confidence intervals (95%CIs) as effect size were calculated by fixed-effect or random-effect models. The overall results indicated that the XRCC1-399G/A polymorphism was marginally associated with cervical carcinoma in Asians: OR (95%CI): 1.16 (1.07, 1.26) in the G/A vs G/G inheritance model, 1.24 (0.87, 1.76)in A/A vs G/G inheritance model, 1.13 (1.01, 1.27) in the dominant inheritance model and 1.18 (0.94, 1.47) in the recessive inheritance model. Subgroup analyses on sample size showed no significant correlation in the small-sample size group but the large-sample size group was consistent with the outcomes of overall meta-analysis. In the subgroup analysis by regions, we only found significant association under the G/A vs G/G inheritance model in the Chinese population. For the non-Chinese populations, no correlation was detected in any genetic inheritance model. In the Asian populations, XRCC1-399G/A gene polymorphism was implied to be associated with cervical carcinoma.
Therapeutic inhibition of SGK1 suppresses colorectal cancer
Xuchun Liang,Chunling Lan,Guanming Jiao,Wencheng Fu,Xuesha Long,Yu An,Kejin Wang,Jinzhe Zhou,Ting Chen,Yongqin Li,Jiahong Xu,Qi Huang,Bin Xu,Junjie Xiao 생화학분자생물학회 2017 Experimental and molecular medicine Vol.49 No.-
Colorectal cancer (CRC) is one of the leading causes of death worldwide. Thus, the development of new therapeutic targets for CRC treatment is urgently needed. SGK1 is involved in various cellular activities, and its dysregulation can result in multiple cancers. However, little is known about its roles and associated molecular mechanisms in CRC. In present study, we found that SGK1 was highly expressed in tumor tissues compared with peri-tumor samples from CRC patients. In vitro experiments revealed that SGK1 overexpression promoted colonic tumor cell proliferation and migration and inhibited cell apoptosis induced by 5-fluorouracil (5-FU), while SGK1 shRNA and inhibitors showed the inverse effects. Using CRC xenograft mice models, we demonstrated that knockdown or therapeutic inhibition of SGK1 repressed tumor cell proliferation and tumor growth. Moreover, SGK1 inhibitors increased p27 expression and promoted p27 nuclear accumulation in colorectal cancer cells, and p27 siRNAs could attenuate the repression of CRC cell proliferation induced by SGK1 inhibitors. Collectively, SGK1 promotes colorectal cancer development via regulation