基因敲除
生物
转移
癌症研究
细胞生长
细胞周期
上皮-间质转换
MMP2型
细胞迁移
PI3K/AKT/mTOR通路
周期素
波形蛋白
细胞周期蛋白D1
细胞
细胞培养
信号转导
癌症
细胞生物学
免疫学
免疫组织化学
遗传学
作者
Fang Liu,Shuping Chen,Yue Yu,Chuanbing Huang,Huijing Chen,Ling Wang,Wanping Zhang,Junxin Wu,Yunbin Ye
出处
期刊:Gene
[Elsevier]
日期:2022-04-01
卷期号:819: 146240-146240
被引量:7
标识
DOI:10.1016/j.gene.2022.146240
摘要
Liver metastasis of colorectal cancer (CRC) remains high mortality and the mechanism is still unknown. Here we investigated the effects of inhibitor of DNA binding 2 (Id2) on growth and liver metastasis of CRC. qPCR and western blotting were used to demonstrate mRNA and protein expressions in Id2-knockdown HCT116 cells. Cell growth was observed by cell proliferation assay, colony formation assay and flow cytometry. Cell migration and invasion were observed with wound healing assay and transwell migration and invasion assay. The effects of Id2 knockdown on tumor growth and liver metastasis in vivo were evaluated respectively with subcutaneous tumor model and colorectal liver metastasis model by injecting HCT116 cells into the mesentery triangle of cecum in mice. Id2 overexpression was found in CRC cell lines. Id2 knockdown resulted in a reduction in the proliferation, colony formation, migration and invasion of HCT116 cells. The suppression of cell proliferation was accompanied by the cell cycle arrest in the G0/G1 phase with down-regulation of Cyclin D1, Cyclin E, p-Cdk2/3, Cdk6, p-p27 and up-regulation of p21 and p27. Id2 knockdown reversed epithelial-mesenchymal transition (EMT) through increasing E-Cadherin and inhibiting N-Cadherin, Vimentin, β-catenin, Snail and Slug. Id2 was also found to inhibit CRC metastasis via MMP2, MMP9 and TIMP-1. Furthermore, Id2 knockdown suppressed CRC liver metastasis in vivo. Id2 promotes CRC growth through activation of the PI3K/AKT signaling pathway, and triggers EMT to enhance CRC migration and invasion.
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