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Feng, Xu,Dong, Chun-Qiang,Shi, Jun-Jie,Zhou, Hua-Fu,He, Wei,Zheng, Bao-Shi Asian Pacific Journal of Cancer Prevention 2012 Asian Pacific journal of cancer prevention Vol.13 No.9
Objective: The conclusions of published reports on the relationship between the glutathione S-transferase M3 (GSTM3) A/B gene polymorphism and the risk of lung cancer are still debated. This meta-analysis was performed to evaluate the association between GSTM3 and the risk of lung cancer. Methods: Association investigations were identified from PubMed, Embase, and Cochrane Library, and eligible studies were included and synthesized using a meta-analysis method. Results: Eight reports were included into this meta-analysis for the association of GSTM3 A/B gene polymorphism and lung cancer susceptibility, covering 1,854 patients with lung cancer and 1,926 controls. No association between the GSTM3 A/B gene polymorphism and lung cancer was found in this meta-analysis (B allele: OR = 1.25, 95% CI: 0.89-1.76, P = 0.20; BB genotype: OR = 1.53, 95% CI: 0.71-3.32, P = 0.28; AA genotype: OR = 0.85, 95% CI: 0.59-1.23, P = 0.39). Conclusions: The GSTM3 A/B gene polymorphism is not associated with lung cancer susceptibility. However, more studies on the relationship between GSTM3 A/B gene polymorphism and the risk of lung cancer should be performed in the future.
Tang, Qing-Feng,Ji, Qing,Tang, Yu,Hu, Song-Jiao,Bao, Yi-Jie,Peng, Wen,Yin, Pei-Hao Asian Pacific Journal of Cancer Prevention 2013 Asian Pacific journal of cancer prevention Vol.14 No.10
Golgi phosphoprotein 2 (GOLPH2) is a very important biomarker in a variety of diseases. Its biological function is not clear, particularly in gastric cancer. To investigate the role of GOLPH2 in human gastric cancer, and determine its effect on the Th1 lymphocyte response, its expression and that of IL-12A were measured by real-time PCR and immunohistochemistry. The relationship between GOLPH2 and IL-12A was analysed statistically. The effect of GOLPH2 on the Th1 lymphocyte response was investigated with an in vitro co-culture system. The results showed that in human gastric cancer, the expression of GOLPH2 was significantly higher and the expression of IL-12A was lower than in normal gastric mucosal tissues, and the expression levels of GOLPH2 and IL-12A were negatively correlated. In addition, obvious down-regulation of the Th1 response was observed when lymphocytes were co-cultured with gastric cancer SGC7901 cells over-expressing GOLPH2. GOLPH2 down-regulated the expression of IL-12A, and inhibited the expression of TNF-${\alpha}$ and IFN-${\gamma}$. The results indicated that GOLPH2 down-regulates the Th1 response via suppression of IL-12A in human gastric cancer, and this might provide a target for the prevention and treatment.
MiR-494-3p Upregulation Exacerbates Cerebral Ischemia Injury by Targeting Bhlhe40
Lingjiang Sun,Dandan Ji,Feng Zhi,Yu Fang,Zigang Zhu,Tong Ni,Qin Zhu,Jie Bao 연세대학교의과대학 2022 Yonsei medical journal Vol.63 No.4
Purpose: Cerebral ischemia is related to insufficient blood supply and is characterized by abnormal reactive oxygen species(ROS) production and cell apoptosis. Previous studies have revealed a key role for basic helix-loop-helix family member e40 (Bhlhe40)in oxidative stress and cell apoptosis. This study aimed to investigate the roles of miR-494-3p in cerebral ischemia/reperfusion(I/R) injury. Materials and Methods: A mouse middle cerebral artery occlusion (MCAO/R) model was established to mimic cerebral ischemiain vivo. Brain infarct area was assessed using triphenyl tetrazolium chloride staining. Oxygen-glucose deprivation/reoxygenation(OGD/R) operation was adopted to mimic neuronal injury in vitro. Cell apoptosis was analyzed by flow cytometry. Therelationship between miR-494-3p and Bhlhe40 was validated by luciferase reporter and RNA immunoprecipitation assays. Results: Bhlhe40 expression was downregulated both in MCAO/R animal models and OGD/R-induced SH-SY5Y cells. Bhlhe40overexpression inhibited cell apoptosis and reduced ROS production in SH-SY5Y cells after OGD/R treatment. MiR-494-3p wasverified to bind to Bhlhe40 and negatively regulate Bhlhe40 expression. Additionally, cell apoptosis and ROS production in OGD/R-treated SH-SY5Y cells were accelerated by miR-494-3p overexpression. Rescue experiments suggested that Bhlhe40 could reversethe effects of miR-494-3p overexpression on ROS production and cell apoptosis. Conclusion: MiR-494-3p exacerbates brain injury and neuronal injury by regulating Bhlhe40 after I/R.