Zhu Jiankang, Liu Chongzhong, Liu Fengyue, Wang Yadong, Zhu Min
Department of Hepatobiliary Surgery, Qilu Hospital, Shandong University, Jinan, China.
Oncol Res. 2016;24(3):137-44. doi: 10.3727/096504016X14611963142218.
PFTK1 is a member of the cyclin-dependent kinase (CDK) family and is upregulated in many types of tumors. However, its expression and role in colon cancer remain unclear. In this study, we aimed to investigate the expression and function of PFTK1 in colon cancer. Our results showed that PFTK1 was highly expressed in colon cancer cell lines. The in vitro experiments demonstrated that knockdown of PFTK1 inhibited the proliferation, migration, and invasion of colon cancer cells as well as the epithelial-to-mesenchymal transition (EMT) progress. Furthermore, knockdown of PFTK1 suppressed the expression of Shh as well as Smo, Ptc, and Gli-1 in colon cancer cells. Taken together, these results suggest that knockdown of PFTK1 inhibited the proliferation and invasion of colon cancer cells as well as the EMT progress by suppressing the Sonic hedgehog signaling pathway. Therefore, these findings reveal that PFTK1 may be a potential therapeutic target for the treatment of colon cancer.
PFTK1是细胞周期蛋白依赖性激酶（CDK）家族的成员，在多种肿瘤中表达上调。然而，其在结肠癌中的表达及作用仍不清楚。在本研究中，我们旨在探究PFTK1在结肠癌中的表达及功能。我们的结果显示，PFTK1在结肠癌细胞系中高表达。体外实验表明，敲低PFTK1可抑制结肠癌细胞的增殖、迁移和侵袭以及上皮-间质转化（EMT）进程。此外，敲低PFTK1可抑制结肠癌细胞中Shh以及Smo、Ptc和Gli-1的表达。综上所述，这些结果表明，敲低PFTK1通过抑制 Sonic hedgehog信号通路来抑制结肠癌细胞的增殖和侵袭以及EMT进程。因此，这些发现揭示PFTK1可能是治疗结肠癌的一个潜在治疗靶点。
