ArticleDiscover oncology2025
Research on the regulatory effects and mechanisms of YES1 on apoptosis and autophagy in cervical cancer cells.
Article in Discover oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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2 authors.
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Abstract
objectiveCervical cancer (CC) is a prevalent form of malignant tumor that impacts the female reproductive system. Its pathogenesis is complex beyond the persistence of high-risk human papillomavirus infection (HR-HPVs). YES1 is a non-receptor tyrosine kinase, yet its specific impact on CC progression remains unclear. We investigated the association with YES1 expression and the malignant biological properties of CC and further explored the potential pathogenic mechanisms mediated by YES1. This offers a possible theoretical basis for the diagnosis, prognostic assessment, and therapeutic targets for CC.
methodsThe YES1 expression levels in CC were analyzed and detected utilizing the TCGA database, immunohistochemistry (IHC), and Western blot. Small interfering RNA was then used to inhibit YES1 expression successfully. Based on this, the functional role of YES1 in CC was explored using a combination of CCK-8 assay, clone formation assay, wound healing assay, Transwell migration and invasion assay, and flow cytometry. The effects of YES1 on proteins implicated in cellular autophagy, apoptosis, and the signaling pathways associated with these processes were investigated using Western blot analysis.
resultsYES1 knockdown reduced cells' ability to proliferate, migrate, and invade, as well as the expression of p62, Bcl-2, PCNA, and PIK3/AKT pathway proteins. Meanwhile, LCII/I, Beclin-1, Bax, Cleaved Caspase-3, and apoptosis rates increased.
conclusionsOur study demonstrated the suppressive impact of YES1 knockdown on CC, which provides a theoretical basis for targeting therapy for CC.
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