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Published on: January 12, 2020
Oncogenic Role of KIF18B Across Human Cancers: A Pan-Cancer Bioinformatic Analysis and Experimental Validation in
Junli Hou1, Xiangrong Shao1, Yawen Zhang1
1Department of Respiratory and Critical Care Medicine, The Affiliated Hospital of Yangzhou University, Yangzhou University, 225000 Yangzhou, Jiangsu, China.
Background:
Identifying oncogenic drivers with broad relevance across multiple cancer types is critical for developing novel therapeutic strategies. Kinesin family member 18B (KIF18B) is involved in mitotic regulation, but its comprehensive role and clinical significance across human malignancies remain poorly understood. This study performed a comprehensive pan-cancer analysis of KIF18B and experimentally validated its role in lung adenocarcinoma (LUAD).
Methods:
We conducted a comprehensive bioinformatic analysis using public databases to evaluate the expression profile, prognostic value, and potential biological functions of KIF18B across various human cancers. Based on these findings, LUAD was selected for further investigation. We evaluated KIF18B protein levels in LUAD cell lines (A549, HCC827, H1975) and compared them to a normal bronchial epithelial cell line (BEAS-2B). Subsequently, KIF18B was silenced in A549 cells using small interfering RNA (siRNA), and its effects on cell proliferation, migration, and invasion were examined using colony formation, wound-healing, and Transwell assays.
Results:
Our analysis across various cancers revealed that KIF18B is markedly overexpressed, including in LUAD, and this high expression correlates with poor prognosis in patients across different cancer types. In line with these bioinformatic results, our experiments confirmed that KIF18B protein levels were elevated in LUAD cell lines compared with normal controls. Functional assays demonstrated that knockdown of KIF18B in A549 cells significantly suppressed colony-forming ability and impaired migratory and invasive capacities.
Conclusions:
This study, integrating pan-cancer bioinformatic analysis with experimental validation, establishes KIF18B as a widely expressed oncogene with significant prognostic value. Our findings in LUAD confirm its crucial role in promoting key malignant phenotypes. Thus, KIF18B emerges as a valuable prognostic biomarker and a potential therapeutic target, not only for LUAD but potentially for a wider array of cancers.
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