Overexpression of KIF18A promotes cell proliferation, inhibits apoptosis, and independently predicts unfavorable prognosis in lung adenocarcinoma

Mar 1, 2019IUBMB life

High levels of KIF18A increase lung adenocarcinoma cell growth, reduce cell death, and predict worse patient outcomes

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Abstract

KIF18A expression was dramatically increased in lung adenocarcinoma tissues compared to normal tissues.

High KIF18A expression is associated with significantly poorer overall survival and recurrence-free survival in lung adenocarcinoma patients.
Increased KIF18A expression may be independently linked to unfavorable survival outcomes.
KIF18A mutations were found in 2.6% of lung adenocarcinoma cases, with increased expression related to genetic amplification rather than DNA methylation.
A total of 339 genes co-expressed with KIF18A were identified, enriched in pathways related to tumors, particularly the cell cycle.
Silencing KIF18A in lung adenocarcinoma cells significantly inhibited cell proliferation, induced apoptosis, and caused cell cycle arrest in the G2/M phase.

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Kinesin family member 18A (KIF18A), as a member of the kinesin superfamily, is significantly overexpressed and abnormally functions in various human cancers. But, its expression profiling in the lung adenocarcinoma (LUAD) remains unclear. In the present work, using the data derived from the Cancer Genome Atlas (TCGA), we assessed the expression pattern and prognostic value of KIF18A in LUAD. In addition, we analyzed the underlying mechanism of its gene dysregulation. Experimental and bioinformatic analysis results showed that KIF18A expression was dramatically increased in LUAD tissues compared with the normal counterparts. Moreover, the patients with high KIF18A expression had significantly poorer overall survival (OS) and recurrence-free survival (RFS). Univariate and multivariate analyses indicated that increased KIF18A expression was independently associated with unfavorable OS and RFS. In addition, by analyzing deep sequencing data from TCGA-LUAD, we found that KIF18A mutation was detected in 2.6% of LUAD cases, and increased KIF18A expression was associated with genetic amplification rather than DNA methylation. Moreover, gene co-expression network analysis revealed that a total of 339 KIF18A co-expressed genes were detected and enriched in several tumor-related pathways, especially cell cycle. Knockdown of KIF18A significantly inhibited cell proliferation in vitro and in vivo. Furthermore, silencing KIF18A induced LUAD cells apoptosis and arrested the cell cycle in the G2/M phase. KIF18A promotes cell proliferation, inhibits apoptosis, and is a valuable prognostic predictor and potential therapeutic target for the patients with LUAD. © 2019 IUBMB Life, 2019.

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Overexpression of KIF18A promotes cell proliferation, inhibits apoptosis, and independently predicts unfavorable prognosis in lung adenocarcinoma

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