首页> 美国卫生研究院文献>International Journal of Clinical and Experimental Pathology >Knockdown of PFTK1 inhibits tumor cell proliferation invasion and epithelial-to-mesenchymal transition in pancreatic cancer
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Knockdown of PFTK1 inhibits tumor cell proliferation invasion and epithelial-to-mesenchymal transition in pancreatic cancer

机译:PFTK1的抑制抑制胰腺癌的肿瘤细胞增殖侵袭和上皮向间质转化

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摘要

PFTK1 was identified as a member of the cyclin-dependent kinase (CDK) family and it is frequently upregulated in many types of tumors. However, its expression and role in pancreatic cancer has not been yet reported. In this study, we aimed to explore the expression and function in pancreatic cancer. The present study verified that PFTK1 was highly expressed in pancreatic cancer cell lines. The in vitro experiments demonstrated that knockdown of PFTK1 inhibited the proliferation, migration and invasion of pancreatic cancer cells as well as the epithelial-to-mesenchymal transition (EMT) progress. Finally, knockdown of PFTK1 inhibited the expression of p-PI3K and p-Akt in pancreatic cancer cells. In summary, the present study has provided further evidence that knockdown of PFTK1 inhibited the proliferation and invasion of pancreatic cancer cells as well as the EMT progress by suppressing the PI3K/Akt signaling pathway. Therefore, these findings reveal that PFTK1 might potentially become a novel strategy for targeting pancreatic cancer.
机译:PFTK1被确定为细胞周期蛋白依赖性激酶(CDK)家族的成员,并且在许多类型的肿瘤中经常被上调。但是,尚未报道其在胰腺癌中的表达和作用。在这项研究中,我们旨在探讨胰腺癌的表达和功能。本研究证实了PFTK1在胰腺癌细胞系中高表达。体外实验表明,敲低PFTK1可以抑制胰腺癌细胞的增殖,迁移和侵袭,以及上皮-间质转化(EMT)的进程。最后,敲低PFTK1抑制了胰腺癌细胞中p-PI3K和p-Akt的表达。总而言之,本研究提供了进一步的证据,即通过抑制PI3K / Akt信号传导途径,敲低PFTK1可以抑制胰腺癌细胞的增殖和侵袭以及EMT进程。因此,这些发现表明PFTK1可能成为靶向胰腺癌的新策略。

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