生物
基因沉默
细胞生长
癌症研究
时钟
小发夹RNA
RNA干扰
基因表达
基因
分子生物学
基因敲除
细胞生物学
核糖核酸
遗传学
作者
Bo Peng,Qi Fang,Xiaoxue Li,Hang Yu,Xuepei Li,Jiang Zhou,Songbai Cheng,Yanyou Liu,Yuhui Wang,Huiling Guo,Jing Xiao,Zhengrong Wang
标识
DOI:10.1080/09291016.2018.1501970
摘要
Colorectal carcinoma (CRC) is one of the most prevalent types of malignancy-associated mortality of the world. Recently, the studies about over-expression circadian locomotor output cycles kaput gene will promote CRC progression and inhibit tumor cell apoptosis in vitro through the AKT-pathway (an antiapoptotic pathway have been reported). However, it remains to be studied the molecular mechanism of proliferation in CRC. In our present study, we attempt to study the clock gene which inhibits proliferation of CRC CT26 cells through p53-dependent pathway when the clock gene is suppressed in the CRC cell line CT26. Lentiviral vector binds to RNA target sequence, knocking down clock genes in CT26 cells with short hairpin RNA. For detecting their proliferation rates, we used CCK8 assay, plate clone formation assay, Western blot and mouse tumorigenicity assay. The results revealed that knocking down the clock gene has a negative effect on CT26 cell proliferation, depicted that low expression of clock gene reduced cylinD1 and c-myc expression, improved P21 and P53 expression in vitro and inhibited the growth of tumor in vivo. In conclusion, while silencing the clock gene can depress CT26 cell growth through p53-dependent pathway and c-myc.
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