癌症研究
结直肠癌
PTEN公司
蛋白激酶B
基因沉默
细胞周期蛋白D1
细胞生长
细胞周期
癌症
PI3K/AKT/mTOR通路
MAPK/ERK通路
NF-κB
生物
化学
医学
信号转导
细胞生物学
内科学
基因
生物化学
遗传学
作者
Yun Hee Kang,Na Ji,Seung Ro Han,Chung Il Lee,Jae Wha Kim,Young Il Yeom,Young Ho Kim,Ho Kyung Chun,Jong Wan Kim,Jin Woong Chung,Dong Kuk Ahn,Hee Gu Lee,Eun Young Song
标识
DOI:10.1016/j.cellsig.2012.06.004
摘要
In our previous study, we reported that endothelial cell specific molecule-1 (ESM-1) was increased in tissue and serum from colorectal cancer patients and suggested that ESM-1 can be used as a potential serum marker for early detection of colorectal cancer. The aim of this study was to evaluate the role of ESM-1 as an intracellular molecule in colorectal cancer. ESM-1 expression was knocked down by small interfering RNA (siRNA) in colorectal cancer cells. Expression of ESM-1 siRNA decreased cell survival through the Akt-dependent inhibition of NF-κB/IκB pathway and an interconnected reduction in phospho-Akt, -p38, -ERK1, -RSK1, -GSK-3α/β and -HSP27, as determined by a phospho-MAPK array. ESM-1 silencing induced G1 phase cell cycle arrest by induction of PTEN, resulting in the inhibition of cyclin D1 and inhibited cell migration and invasion of COLO205 cells. Consistently, ESM-1 overexpression in HCT-116 cells enhanced cell proliferation through the Akt-dependent activation of NF-κB pathway. In addition, ESM-1 interacted with NF-κB and activated NF-κB promoter. This study demonstrates that ESM-1 is involved in cell survival, cell cycle progression, migration, invasion and EMT during tumor invasion in colorectal cancer. Based on our results, ESM-1 may be a useful therapeutic target for colorectal cancer.
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