ArticleNaunyn-Schmiedeberg's archives of pharmacology2026
Exploring betanin regulatory impact on TGF-β and PI3K/AKT pathways in oral cancer.
Article in Naunyn-Schmiedeberg's archives of pharmacology, 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
Oral squamous cell carcinoma (OSCC) presents ongoing clinical difficulties due to its frequent recurrence and unfavorable prognosis. Betanin (BTN) is recognized for its potent antioxidant and anticancer properties; however, its specific molecular mechanisms, particularly those related to the apoptotic and TGF-β/PI3K-Akt signalling pathways, remain partially unexplored. An in vivo study was performed using 7,12-dimethylbenz[a]anthracene (DMBA)-induced OSCC in hamsters, where the expression patterns of PI3K, Akt, Bax, Bcl-2, Caspase-3, Caspase-9, mutant p53, TGF-β RI & RII, SMAD-2, SMAD-4, and SMAD-7 were examined through immunohistochemistry, Western blot, and qRT-PCR, with a focus on PI3K/Akt and TGF-β signaling pathways. BTN, administered in vivo, attenuated tumor progression in OSCC-afflicted hamsters in a dose-dependent manner, inhibiting growth-regulatory signalling nodes such as PI3K, Akt, Bcl-2, mutant p53, TGF-β RI, TGF-β RII, SMAD-2, and SMAD-4, while promoting the expression of apoptotic proteins SMAD-7, Bax, Caspase-3, and Caspase-9. BTN exhibits multi-targeted anticancer potential in OSCC by modulating the expression of with key apoptotic (Bax, Bcl-2, Caspases-3 & 9, mutant p53) and growth-regulatory signalling nodes PI3K, Akt, TGF-β RI, TGF-β RII, SMAD-2, 4, and 7. Our previous molecular docking study directly engages the aforementioned proteins. As a result, the current experimental framework identifies BTN as a potential chemopreventive agent, meriting additional mechanistic and therapeutic research in the context of oral cancer.
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