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G9a regulates tumorigenicity and stemness through genome-wide DNA methylation reprogramming in non-small cell lung cancer

机译:G9A通过非小细胞肺癌的基因组DNA甲基化调节致瘤性和茎致致肿瘤性和茎

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摘要

Targeting G9A decreased stemness and in vitro cell proliferation of tumor initiating cells (TICs) derived from NSCLC patients. a Basal level of G9A expression and corresponding H3K9Me2 level in tumor spheres of tumor-initiating cells (TICs) isolated from primary non-small lung cancer tissues determined by western blot. b G9A expression in FACS-sorted CD133+ and CD133− cells in two TICs. c Expression level of CD133, and H3K9Me2 following G9A knockdown are shown. G9A knockdown resulted in decreased sphere forming (10X magnification) (d), and cell proliferation capacity (e) of TICs in vitro. Treatment of TICs with G9A inhibitor UNC0642 resulted in decreased sphere forming (× 10 magnification) (f) and cell proliferation (g) capacity in vitro. (For t test: *P < 0.05, **P < .01, and ***P < 0.001)
机译:靶向G9A源自NSCLC患者肿瘤引发细胞(TICS)的茎秆和体外细胞增殖降低。由蛋白质印迹测定的原发性非小肺癌组织中分离的肿瘤发起细胞(TICS)肿瘤球体的G9A表达和相应H3K9ME2水平的基础水平。 B G9A在FACS中的表达 - 分类中的CD133 +和CD133细胞。显示CD133的C表达水平和G9A敲低后的H3K9ME2。 G9A敲低导致体外球体形成(10倍倍率)(D)和细胞增殖能力(e)的细胞增殖能力(e)。用G9A抑制剂UNC0642治疗TIC导致球体成形(×10倍率)(F)和体外细胞增殖(G)容量降低。 (对于T检验:* P <0.05,** P <.01,和*** P <0.001)

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