Background: Lung cancer remains the leading cause of cancer-related death worldwide. The human gene (PTEN induced kinase 1, Park6), an important gene for Parkinson's disease, was found to be associated with tumor development although the molecular mechanisms underlying this relationship remain largely unknown.
Objective: To analyze the clinical value and molecular mechanism of in non-small cell lung cancer (NSCLC).
Materials And Methods: Western blot, qRT-PCR and Immunohistochemistry were employed to determine the levels of in 87 paired NSCLC tissues, Oncomine and TCGA databases were also used for the evaluation of expression and prognosis of . The mitophagy, proliferation, migration, invasion, and apoptosis abilities of A549 and H1975 cells were detected, and the autophagy-related proteins in the cells were also determined.
Results: Immunohistochemical staining revealed higher expression in tumor tissues, which was strongly linked to the tumor-node-metastasis classification. Survival analysis of 1085 NSCLC patients also revealed that low expression levels were associated with significantly longer overall survival. Univariate and multivariate analyses indicated that expression was an independent predictor of overall survival among patients with NSCLC. We also evaluated the influence of deficiency in NSCLC cell lines (A549 and H1975), which revealed significant suppression of migration capability and cell viability, as well as a significantly elevated apoptosis ratio. In cells with stable interference of expression, dysfunctional mitochondria accumulated while autophagy was inhibited, which indicated that cell activity suppression was mediated by the accumulation of dysfunctional mitochondria. The suppression of migration and autophagy was reversed in cells that overexpressed .
Conclusion: Our results suggest that PINK1 may be a potential therapeutic target and prognostic biomarker in NSCLC.
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| http://dx.doi.org/10.2147/CMAR.S262466 | DOI Listing |
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