Open AccessCD 155 knockdown promotes apoptosis via AKT /Bcl‐2/Bax in colon cancer cells
Author(s) -
Zheng Qianqian,
Wang Biao,
Gao Jian,
Xin Na,
Wang Wei,
Song Xiaowen,
Shao Yue,
Zhao Chenghai
Publication year - 2018
Publication title -
journal of cellular and molecular medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.44
H-Index - 130
eISSN - 1582-4934
pISSN - 1582-1838
DOI - 10.1111/jcmm.13301
Subject(s) - gene knockdown , colorectal cancer , apoptosis , cancer research , cell growth , metastasis , small hairpin rna , protein kinase b , cell migration , cancer , cell adhesion molecule , programmed cell death , cell , biology , signal transduction , microbiology and biotechnology , biochemistry , genetics
CD 155, one of the nectin‐like molecule family members, is involved in cell adhesion and motility. CD 155 is overexpressed in several human cancers, but its role in proliferation and apoptosis of colorectal cancer remains unclear. We found that CD 155 was up‐regulated in colorectal cancer tissues. CD 155 knockdown via sh RNA lentiviruses inhibited colon cancers cell migration and invasion, with a reduction in the expression of FAK , Src and MMP ‐2. CD 155 down‐regulation also suppressed colon cancer cell proliferation, accompanied by changing expressions of some molecules related to cell cycle. Finally, CD 155 knockdown increased the expression ratio between Bax and Bcl‐2, resulting in a significant increase in colon cancer cell apoptosis. Taken together, these results demonstrate that CD 155 is involved in not only migration and invasion but also proliferation and survival abilities of colon cancer cells, suggesting that CD 155 is one of key molecules promoting the growth and metastasis of colorectal cancer.