Knockdown of PLK1 inhibits invasion and promotes apoptosis in glioma cells through regulating autophagy.

Abstract

Polo like kinase 1 (PLK1), an oncogene, is a ubiquitously expressed serine/threonine protein kinase. We aimed at investigating the role of PLK1 in glioma. Clinical glioma specimens were obtained from Zhejiang Hospital (Hangzhou, Zhejiang, China). The mRNA and protein levels of PLK1 in glioma tissues and different glioma cells were analyzed by Real-time PCR and Western blot, respectively. The expression of PLK1 protein in glioma tissues was also determined by immunohistochemistry staining. Then, the effect of PLK1 on cell proliferation and apoptosis of U251 and U87 cells was analyzed by using CCK-8 assay and Annexin V/PI staining, respectively. Furthermore, the migration and invasion of glioma cells were examined by transwell assay. Finally, the protein levels of autophagy indicators LC3-II, ATG5 and p-p70 S6 in U251 and U87 cells were detected by Western blot, and the expression of E-cadherin, vimentin and MMP9 and apoptosis associated indicators Bax, cleaved caspase-3 and Bcl-2 in U251 cells were also determined using Western blot. PLK1 was upregulated in glioma tissues and cells. Knockdown of PLK1 significantly inhibited cell proliferation, migration, invasion, and induced apoptosis of U87 and U251 glioma cells. Furthermore, the data demonstrated that knockdown of PLK1 significantly elevated expression of cleaved caspase-3, BIM, BAX, and E-cadherin, and reduced expression of MMP9, ATG5 and LC3-II in U251 and U87 cells. Additionally, we found that knockdown of PLK1 can inhibit autophagy in glioma cells. Knockdown of PLK1 can inhibit the glioma development by suppressing the autophagy and enhancing the apoptosis of glioma cells. PLK1 may be a potential therapeutic target in gliomas.