Pancancer analysis of SKA1 mutation and its association with the diagnosis and prognosis of human cancers

This study aims to explore the role of SKA1 in cancer diagnosis and prognosis and to investigate the mechanism by which SKA1 affects the malignant behaviors of ovarian cancer. Herein, we analyzed the oncogenic role of SKA1 at pan-cancer level by multiple informatics databases and verified the analys...

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Veröffentlicht in:Genomics (San Diego, Calif.) Calif.), 2023-03, Vol.115 (2), p.110554-110554, Article 110554
Hauptverfasser: Lan, Hua, Yuan, Jing, Zhang, Rui, Jiang, Biyao, Li, Qiaofen, Huang, Zongyan, Chen, Peiling, Xiang, Huimin, Zeng, Xiangyang, Xiao, Songshu
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Sprache:eng
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Zusammenfassung:This study aims to explore the role of SKA1 in cancer diagnosis and prognosis and to investigate the mechanism by which SKA1 affects the malignant behaviors of ovarian cancer. Herein, we analyzed the oncogenic role of SKA1 at pan-cancer level by multiple informatics databases and verified the analysis by in vitro experiments. As a result, SKA1 was upregulated across cancers and was related to poor clinical outcome and immune infiltration. Specifically, the constructed nomogram showed superior performance in predicting the prognosis of epithelial ovarian cancer patients. Furthermore, the in vitro experiments revealed that silencing SKA1 significantly inhibited the proliferation, migratory ability and enhanced the cisplatin sensitivity of ovarian cancer cells. Therefore, we explored the oncogenic and potential therapeutic role of SKA1 across cancers through multiple bioinformatic analysis and revealed that SKA1 may promote ovarian cancer progression and chemoresistance to cisplatin by activating the AKT-FOXO3a signaling pathway. •This study provides a global introduction of SKA1 in pan-cancers using multi-omics database.•SKA1 is correlated with multiple immune cells and molecules, indicating the potential role in regulating tumor immune.•We further verified that SKA1 serve as an important oncogene and promote cancer cell progression through Akt/Foxo3a pathway.
ISSN:0888-7543
1089-8646
DOI:10.1016/j.ygeno.2022.110554