Lentivirus-mediated RNA interference of tripartite motif 68 inhibits the proliferation of colorectal cancer cell lines SW1116 and HCT116 in vitro
Lentivirus-mediated RNA interference of tripartite motif 68 inhibits the proliferation of colorectal cancer cell lines SW1116 and HCT116 in vitro
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DOI：
10.3892/ol.2017.5787
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发表时间：
2017-04-01
期刊：
影响因子：
2.9
通讯作者：
Fu, Chuangang
中科院分区：
文献类型：
--
作者：
Tan, Zhen;Liu, Xiaoshuang;Fu, Chuangang
结直肠癌是世界上最常见的癌症类型之一。已有研究表明TRIM蛋白的某些成员参与了大肠癌的发生调控，但TRIM 68在大肠癌中的功能尚不清楚。为了研究TRIM 68在结直肠癌SW 1116和HCT 116细胞系中的作用，本研究进行了慢病毒介导的TRIM 68敲除，并证明TRIM 68的缺失显著抑制结直肠癌细胞增殖和集落形成能力。细胞周期停滞于G 0/G1期，细胞周期积累于亚G1期，表明TRIM 68可能参与了大肠癌发生的调控。结果显示TRIM 68在调节结直肠癌细胞有丝分裂中的重要作用，并表明TRIM 68可能是一个有前途的治疗靶点。
Colorectal cancer is one of the most common types of cancer worldwide. Previous studies have revealed that certain members of tripartite motif (TRIM) proteins are involved in carcin ogenesis regulation, but little is known about the function of TRIM68 in human colorectal cancer. To investigate the role of TRIM68 in colorectal cancer SW1116 and HCT116 cell lines, the present study conducted lentivirus-mediated knockdown against TRIM68 and demonstrated that depletion of TRIM68 notably inhibits colorectal cancer cell proliferation and colony formation ability. Cell cycle arrest in the G0/G1 phase and cycle accumulation in sub-G1 phase provided evidence that TRIM68 may participate in the regulation of colorectal cancer tumorigenesis. The results revealed the significant role of TRIM68 in regulating colorectal cancer cell mitosis and indicated that TRIM68 may be a promising therapeutic target.