ArticleFunctional & integrative genomics2025
CircSHPRH inhibits malignancy progression of head and neck squamous cell carcinoma by regulating PI3K/AKT/mTOR signaling pathway.
Article in Functional & integrative genomics, 2025. 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
backgroundHead and neck squamous cell carcinoma (HNSCC) stands as a significant global health concern, marked by its substantial impact on both morbidity and mortality rates. Although previous studies have suggested that circular RNAs (circRNAs) may influence HNSCC progression, the underlying mechanisms remain largely unclear.
methodsIn this study, we first used quantitative real-time polymerase chain reaction (qRT-PCR) to measure the expression levels of circSHPRH in HNSCC tissues and cell lines. Subsequently, we assessed its impact on cell proliferation, migration, invasion, and apoptosis using CCK-8 assays, colony formation assays, wound healing assays, Transwell assays, and flow cytometry. Additionally, we investigated the molecular mechanisms by which circSHPRH exerts its effects, focusing on the phosphatidylinositol-3-kinase/protein kinase B/mammalian target of rapamycin (PI3K/AKT/mTOR) signaling pathway. In vivo experiments were conducted using a xenograft tumor model in nude mice to validate the tumor-suppressive effects of circSHPRH.
resultsOur results demonstrated a significant downregulation of circSHPRH in HNSCC tissues and cell lines compared to their normal counterparts. Overexpression of circSHPRH in HNSCC cells led to a marked reduction in cell proliferation, migration, and invasion, while promoting apoptosis. Mechanistically, we found circSHPRH exerts its tumor-suppressive effects by suppressing the PI3K/AKT/mTOR signaling pathway. This finding was corroborated by in vivo experiments in nude mice, where an upregulation of circSHPRH led to a reduction in tumor growth in HNSCC.
conclusionCircSHPRH may play a pivotal role in attenuating the growth and metastasis of HNSCC, both at the cellular level and in animal models, by disrupting the PI3K/AKT/mTOR signaling axis.
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