Lentivirus-mediated knockdown of NOB1 suppresses the proliferation of colon cancer cells.
NOB1 is important for ribosome biogenesis and protein degradation. Previous studies showed that it could regulate the growth and colony-formation ability of ovarian, breast and hepatocellular carcinoma cells. However, its function in colon cancer cells is largely unknown. In this study, we found that NOB1 could express in 6 different colon cancer cell lines. Lentivirus-mediated shRNA targeted NOB1 could suppress the endogenous gene expression. NOB1 depletion significantly inhibited cell proliferation and colony formation ability, as determined by MTT and colony formation assays. Flow cytometry analysis showed NOB1 silencing arrested cell cycle in G0 / G1 phase. Moreover, the percentage of cells at sub-G1 phase dramatically increased after NOB1 knockdown. These results indicate that NOB1 may play an important role in the growth and tumorigensis of colon cancer and knockdown of NOB1 may be a potential therapeutic method for colon cancer in the future.
Y
Y
Liu
H
H
Huang
B
B
Yuan
L Y
LY
Zhuang
T P
TP
Luo
Q
Q
Zhang
D002453:Cell Cycle / Q000235:genetics*; D045744:Cell Line, Tumor; D049109:Cell Proliferation / Q000235:genetics*; D003110:Colonic Neoplasms / Q000235:genetics* / Q000473:pathology*; D015972:Gene Expression Regulation, Neoplastic / Q000235:genetics; D055785:Gene Knockdown Techniques / Q000379:methods*; D006801:Humans; D016086:Lentivirus / Q000235:genetics*