Overexpression of PER3 Inhibits Self-Renewal Capability and Chemoresistance of Colorectal Cancer Stem-Like Cells via Inhibition of Notch and β-Catenin Signaling.
作者： Feng Zhang , Hong Sun , Sai Zhang , Xin Yang , Guogang Zhang
DOI: 10.3727/096504016X14772331883976
关键词:
摘要: PER3, a circadian clock gene, plays an important role in colorectal cancer, but its action and underlying mechanism cancer stem-like cells (CSCs) remain unclear. In this study, the CSCs were enriched HCT-116 sphere-forming cells, expressing lower levels of stem cell markers CD133, CD44, LGR5, SOX2 compared with cells. A drug-resistant strain from was established. Western blot qRT-PCR analysis showed that PER3 downregulated HCT-116. Overexpression could strengthen 5-FU-induced inhibitory effects on CSCs, knockdown decreased inhibition CSCs. addition, overexpression resulted reduced colony formation efficiency soft agar medium self-renewal efficiency. Inversely, enhanced stemness Notch1, Jagged1, β-catenin, c-Myc, LGR5 When Notch or β-catenin signaling inhibited, chemoresistance capability decreased. It confirmed can reduce via signaling. Our results reveal critical maintaining may be promising target for elimination
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