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- 저자 : Baohui Han (검색결과 2 건)
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Potential Antitumor Activity of SIM-89 in Non-Small Cell Lung Cancer Cells
Jun Pei,Baohui Han,Tianqing Chu,Minhua Shao,Jiajun Teng,Huifang Sha,Aiqing Gu,Rong Li,Jialin Qian,Weifeng Mao,Ying Li 연세대학교의과대학 2017 Yonsei medical journal Vol.58 No.3
Purpose: c-Met and its ligand, hepatocyte growth factor (HGF), play a critical role in oncogenesis and metastatic progression. The aim of this study was to identify inhibited enzymogram and to test the antitumor activity of SIM-89 (a c-Met receptor tyrosine kinaseinhibitor) in non-small cell lung cancer. Materials and Methods: Z’-LYTE kinase assay was employed to screen the kinase enzymogram, and mechanism of action (MOA) analysis was used to identify the inhibited kinases. Cell proliferation was then analyzed by CCK8 assay, and cell migration was determinedby transwell assay. The gene expression and the phosphorylation of c-Met were examined by realtime-PCR and western blotting, respectively. Finally, the secretion of HGF was detected by ELISA assay. Results: c-Met, activated protein kinase (AMPK), and tyrosine kinase A (TRKA) were inhibited by SIM-89 with the IC50 values of 297 nmol/L, 1.31 μmol/L, and 150.2 nmol/L, respectively. SIM-89 exerted adenosine triphosphate (ATP) competitive inhibition on c-Met. Moreover, the expressions of STAT1, JAK1, and c-Met in H460 cells were decreased by SIM-89 treatment, and c-Met phosphorylationwas suppressed in A549, H441, H1299, and B16F10 cells by the treatment. In addition, SIM-89 treatment significantly decreased the level of HGF, which accounted for the activation of c-Met receptor tyrosine kinase. Finally, we showed cell proliferationinhibition and cell migration suppression in H460 and H1299 cells after SIM-89 treatment. Conclusion: In conclusion, SIM-89 inhibits tumor cell proliferation, migration and HGF autocrine, suggesting it’s potential antitumoractivity.
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Novel blood-based hypomethylation of SH3BP5 is associated with very early-stage lung adenocarcinoma
Qiao Rong,Zhong Runbo,Liu Chunlan,Di Feifei,Zhang Zheng,Wang Ling,Xu Tian,Wang Yue,Dai Liping,Gu Wanjian,Han Baohui,Yang Rongxi 한국유전학회 2022 Genes & Genomics Vol.44 No.4
Background: Early detection is essential to improve the survival of lung cancer (LC). The quantitative measurement of specific DNA methylation changes in the peripheral blood could provide an efficient strategy for the detection of early cancer. Objective: We applied a candidate approach and assess the association between blood-based SH3BP5 methylation and the risk of lung adenocarcinoma (LUAD) in a case-control cohort. Methods: The methylation level of four CpG sites in the promoter of SH3BP5 gene was quantitatively determined by mass spectrometry in 171 very early-stage LUAD patients (93.6% LUAD at stage I) and 190 age and gender-matched controls. The logistic regression and non-parametric tests were used for the statistical analyses. Results: We observed a significant association between decreased methylation of SH3BP5_CpG_4 in the peripheral blood and increased risk of LUAD (odds ratio (OR) per-10% methylation = 1.51, P = 0.006, FDR = 0.024), and even for the LUAD at stage I (OR per-10% methylation = 1.53, P = 0.006, FDR = 0.024). Moreover, the lower quartile of SH3BP5_CpG_4 methylation was correlated with increased risk for LUAD with a P trend of 0.011. Further investigation disclosed that the hypomethylation of SH3BP5_CpG_4 was mostly associated with LUAD in younger subjects (OR per-10% methylation = 2.02, P = 0.010, age < 55 years old) and probably could be enhanced by advance stage. Conclusion: Our study revealed an association between blood-based SH3BP5 hypomethylation and very early-stage LUAD, which provides a novel support for the blood-based methylation signatures as a potential marker for the evaluation of cancer risk.
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