COL3A1促进结直肠癌生长及潜在调控机制

 目的  研究COL3A1对结直肠癌发生发展的影响及潜在机制。方法  使用小干扰RNA(small interfering RNA,siRNA)瞬时干扰方法下调细胞COL3A1表达,使用瞬时过表达方法上调COL3A1表达;使用Western blot检测干扰或过表达COL3A1后蛋白质表达水平及Akt/mTOR通路蛋白质水平的变化;使用MTT法、细胞计数法及平板克隆形成法检测细胞增殖的变化。结果  COL3A1过表达后,结直肠癌细胞增殖速度显著上升,可激活Akt/mTOR信号通路并上调下游基因的表达,沉默COL3A1后,结直肠癌细胞增殖速度显著下降,并可显著抑制肿瘤细胞克隆的形成。结论  COL3A1在结直肠癌中发挥促肿瘤生长的作用,可能成为结直肠癌临床检测和治疗的潜在靶标。

COL3A1 promotes colorectal cancer growth and its potential regulation mechanism

Objective  To investigate the effect of COL3A1 on the occurrence and development of colorectal cancer and its potential regulation mechanism.Methods  COL3A1 expression was down-regulated by small interfering RNA (siRNA) and was up-regulated by transient overexpression.The levels of COL3A1 protein and Akt/mTOR proteins were detected by Western blot.Cell proliferation was detected by MTT assay,cell counting and plate clone formation assay.Results  Over expression of COL3A1 increased the proliferation rate of colorectal cancer cells significantly and activated the Akt/mTOR signaling pathway with increasing the expression of downstream genes.The proliferation rate and the flat plate clone formation of colorectal cancer cells were significantly inhibited with COL3A1 silencing.Conclusions  COL3A1 played an important role in promoting the growth of colorectal cancer,which suggested that it may be a potential target for clinical detection and treatment of colorectal cancer.