Overexpression of KIF20A confers malignant phenotype of lung adenocarcinoma by promoting cell proliferation and inhibiting apoptosis

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.

The Clinical Significance and Potential Molecular Mechanisms of Synaptojanin 2 in Lung Adenocarcinoma

“…Therefore, we argue that SYNJ2 may act with CEP55 to promote the proliferation, migration, and invasion of LUAD. KIF20A also has been detected as being overexpressed in numerous types of human malignancies, including LUAD, and its overexpression can stimulate LUAD cells' proliferation [48]. Matching our results, Sun et al [49] also reported that NDC80 expression was strikingly elevated in LUAD and related to prognosis.…”

Unravelling the Role of miR-20b-5p, CCNB1, HMGA2 and E2F7 in Development and Progression of Non-Small Cell Lung Cancer (NSCLC)

“…Consistently, Kaplan-Meier analysis in our study has shown that NSCLC patients with higher expression of KIF20A have a shorter OS and is also associated with clinical stages. In-vitro studies have identified the mechanism by which KIF20A promotes tumorigenesis, i.e., cell cycle dysregulation and inhibition of apoptosis [44]. In addition, cancer cells overexpressing KIF20A can be recognized by host immune system and hence KIF20A-derived peptides can be used as immunotherapeutic agents.…”

KIF20A Predicts Poor Survival of Patients and Promotes Colorectal Cancer Tumor Progression through the JAK/STAT3 Signaling Pathway

“…Given that KIF20A can directly interact with Rab6 small GTPase-binding protein and participate in the dynamics of the Golgi apparatus, it was first named Rab6-binding kinesin (RAB6KIFL) [ 8 , 9 ]. Recently, several studies have demonstrated that KIF20A may play an important role in the development and progression of many different types of cancer, including melanoma [ 10 ], breast cancer [ 11 , 12 ], nasopharyngeal cancer [ 13 ], pancreatic cancer [ 14 – 16 ], hepatocellular carcinoma [ 17 ], and lung cancer [ 18 , 19 ]. Therefore, KIF20A is regarded as a novel tumor-associated gene.…”

“…Zhao et al confirmed that KIF20A is highly expressed in lung adenocarcinoma and may serve as an independent prognostic factor for OS. Moreover, knockdown of KIF20A could inhibit cell proliferation through G1 phase arrest and induce apoptosis [18]. In ovarian clear-cell carcinoma, high KIF20A expression may contribute to disease progression, which is principally attributable to its asymptomatic intraperitoneal dissemination with or without distant metastases to parenchymal organs [38].…”