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RNA干扰抑制PFTK1表达可抑制人非小细胞肺腺癌细胞的增殖和侵袭。

Knockdown of PFTK1 Expression by RNAi Inhibits the Proliferation and Invasion of Human Non-Small Lung Adenocarcinoma Cells.

作者信息

Liu Mei-Han, Shi Shao-Min, Li Kai, Chen En-Qi

机构信息

Department of Ultrasonography, China-Japan Union Hospital of Jilin University, Changchun, Jilin Province, China.

出版信息

Oncol Res. 2016;24(3):181-7. doi: 10.3727/096504016X14635761799038.

DOI:10.3727/096504016X14635761799038
PMID:27458099
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7838604/
Abstract

PFTK1 (PFTAIRE protein kinase 1), also named CDK14 (cyclin-dependent kinase 14), is a member of the cell division cycle 2 (CDC2)-related protein kinase family. It is highly expressed in several malignant tumors. However, the role of PFTK1 in the progression of non-small cell lung cancer (NSCLC) is still elusive. In this study, we aimed to explore the expression and function of PFTK1 in NSCLC cells. Our results showed that PFTK1 was significantly upregulated in human NSCLC cell lines. Silencing the expression of PFTK1 inhibited the proliferation of NSCLC cells. In addition, silencing the expression of PFTK1 endowed NSCLC cells with decreased migration and invasion abilities, as well as epithelial-mesenchymal transition (EMT) progress in A549 cells. A mechanistic study showed that knockdown of PFTK1 inhibited the expression of β-catenin, cyclin D1, and c-Myc in A549 cells. In summary, we report that small interfering RNA (siRNA)-PFTK1 might inhibit the proliferation and invasion of NSCLC cells by suppressing the Wnt/β-catenin signaling pathway. Therefore, PFTK1 may represent a novel therapeutic target for the treatment of NSCLC.

摘要

PFTK1（PFTAIRE蛋白激酶1），也被称为CDK14（细胞周期蛋白依赖性激酶14），是细胞分裂周期2（CDC2）相关蛋白激酶家族的成员。它在多种恶性肿瘤中高表达。然而，PFTK1在非小细胞肺癌（NSCLC）进展中的作用仍不清楚。在本研究中，我们旨在探讨PFTK1在NSCLC细胞中的表达及功能。我们的结果显示，PFTK1在人NSCLC细胞系中显著上调。沉默PFTK1的表达可抑制NSCLC细胞的增殖。此外，沉默PFTK1的表达使NSCLC细胞的迁移和侵袭能力降低，同时抑制了A549细胞中的上皮-间质转化（EMT）进程。机制研究表明，敲低PFTK1可抑制A549细胞中β-连环蛋白、细胞周期蛋白D1和c-Myc的表达。总之，我们报道小干扰RNA（siRNA）-PFTK1可能通过抑制Wnt/β-连环蛋白信号通路来抑制NSCLC细胞的增殖和侵袭。因此，PFTK1可能是治疗NSCLC的一个新的治疗靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d50d/7838604/e41cb43ee5b2/OR-24-181-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d50d/7838604/1832ff319653/OR-24-181-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d50d/7838604/2bafc1cf657d/OR-24-181-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d50d/7838604/c2d0fc39a6c8/OR-24-181-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d50d/7838604/3a25ac2bff7c/OR-24-181-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d50d/7838604/e41cb43ee5b2/OR-24-181-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d50d/7838604/1832ff319653/OR-24-181-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d50d/7838604/2bafc1cf657d/OR-24-181-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d50d/7838604/c2d0fc39a6c8/OR-24-181-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d50d/7838604/3a25ac2bff7c/OR-24-181-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d50d/7838604/e41cb43ee5b2/OR-24-181-g005.jpg

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