ArticleMolecular and cellular biochemistry2026
SKA1 plays a tumor-promoting role in colorectal cancer: coupling TAF1‑dependent transcription with RPL8 interaction.
Article in Molecular and cellular biochemistry, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Colorectal cancer (CRC), one of the most prevalent and lethal malignancies worldwide, is driven by complex genetic and molecular alterations. In this study, we aimed to identify the functional role of spindle and kinetochore associated complex subunit 1 (SKA1) and uncover its novel mechanism that promotes CRC progression. Bioinformatic TCGA analysis, paired clinical tissue detection and immunohistochemistry confirmed the elevated SKA1 expression in CRC lesions; high SKA1 expression correlates with unfavorable overall survival in CRC patients. Besides, SKA1 overexpression expedited proliferation, accelerated cell cycle G1/S transition, and enhanced migration and invasion, while suppressing apoptosis in CRC cells, which could be reversed by SKA1 silencing. In vivo, SKA1 silencing suppressed tumor growth in a LoVo cell subcutaneous xenograft nude mouse model, whereas SKA1 overexpression accelerated tumor progression in those derived from SW480 cells. Furthermore, ribosomal protein L8 (RPL8) was identified to interact with SKA1 and mediate the tumor-promoting effects. Silencing RPL8 abolished SKA1-driven proliferation and survival advantages, indicating its downstream role. Subsequently, our studies validated that TATA-box binding protein associated factor 1 (TAF1) directly binds to the SKA1 promoter and transcriptionally activates SKA1 expression. Loss of TAF1 attenuated CRC cell proliferation and invasion, whereas SKA1 overexpression rescued these inhibitory effects. Besides, the truncation mutation of the TAF1 N-terminal TAND domain abolished its binding to the SKA1 promoter and eliminated its transactivation capacity. Collectively, our findings define a novel TAF1/SKA1/RPL8 regulatory axis that critically drives CRC progression, highlighting SKA1 as a potential target and providing new insights into the mechanisms underlying CRC development and progression.
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