Abstract
Increasing studies showed that kinesin family member 20A (KIF20A) was overexpessed in several types of cancer, and its overexpression correlated with the oncogenesis and prognosis of cancers. However, little is known about the role of KIF20A in lung adenocarcinoma (LUAD). In this study, we employed the bioinformatics analysis to identify the upregulation of KIF20A in LUAD, then verified the results in human tumor specimens and LUAD cell lines. Compared with normal lung tissues, a ubiquitous upregulation of KIF20A was observed in LUAD tissues by immunohistochemistry (IHC) as well as TCGA analysis. Higher expression of KIF20A was significantly associated with more advanced clinicopathological features and shorter overall survival (OS). Moreover, multivariate Cox regression analysis revealed that KIF20A was an independent prognostic factor for OS. The expression of KIF20A was significantly elevated in LUAD cell lines. After silencing KIF20A, lung cancer cell cycle arrested in G1 phase and apoptosis increased. The same results were observed in vivo. Thus, our study demonstrated that KIF20A might confer malignant phenotype to LUAD by regulating cell proliferation and apoptosis, providing a new potential biomarker for clinical treatment of LUAD.
Highlights
Lung adenocarcinoma (LUAD), the most common subtype of lung cancer, is one of the leading causes of the highest cancer-related morbidity and mortality worldwide.[1]
Kinesin family member 20A (KIF20A) is a member of the Kinesin superfamily containing a conserved motor domain which binds to microtubules to generate the energy required for protein movement.[3]
For the first time we confirmed the oncogenic role of KIF20A in LUAD
Summary
Lung adenocarcinoma (LUAD), the most common subtype of lung cancer, is one of the leading causes of the highest cancer-related morbidity and mortality worldwide.[1]. In 2005, for the first time, the oncogenic properties of KIF20A was confirmed in pancreatic cancer, and downregulating KIF20A could significantly decrease tumor cell proliferation.[6]. KIF20A was identified as one of the co-upregulated genes among four independent lung cancer gene microarray datasets downloaded from the Gene Expression Omnibus (GEO) database. Both in vitro and in vivo experiments showed that KIF20A might confer malignant phenotype to LUAD by promoting cell proliferation and inhibiting apoptosis. Our results suggested that KIF20A could serve as a novel biomarker with therapeutic potential for treatment of LUAD
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