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Exploring betanin regulatory impact on TGF-β and PI3K/AKT pathways in oral cancer

Ramachandhiran Duraisamy1, Vinothkumar Veerasamy2, Vaitheeswari Balakrishnan1

  • 1Department of Biochemistry and Biotechnology, Faculty of Science, Annamalai University, Chidambaram, Annamalainagar, Tamil Nadu, 608002, India.

Naunyn-Schmiedeberg'S Archives of Pharmacology
|July 23, 2026
PubMed

Insights

Betanin (BTN) shows promise in preventing oral cancer by inhibiting tumor growth and promoting apoptosis. This study explored its effects on key signaling pathways involved in oral squamous cell carcinoma (OSCC).

Area of Science:

  • Oncology
  • Molecular Biology
  • Pharmacology

Background:

  • Oral squamous cell carcinoma (OSCC) has a high recurrence rate and poor prognosis, necessitating novel therapeutic strategies.
  • Betanin (BTN), a natural compound, possesses antioxidant and anticancer properties, but its precise molecular mechanisms in OSCC require further elucidation.
  • Understanding BTN's impact on apoptotic and TGF-β/PI3K-Akt signaling pathways is crucial for its therapeutic development.

Purpose of the Study:

  • To investigate the in vivo chemopreventive potential of Betanin (BTN) against 7,12-dimethylbenz[a]anthracene (DMBA)-induced oral squamous cell carcinoma (OSCC) in hamsters.
  • To elucidate the molecular mechanisms of BTN's action by examining its effects on key proteins within the PI3K/Akt and TGF-β signaling pathways.
  • To assess BTN's influence on apoptosis-related proteins and growth-regulatory signaling nodes in the context of OSCC.

Main Methods:

  • An in vivo study utilizing a hamster model of DMBA-induced OSCC.
  • Quantitative analysis of protein expression using immunohistochemistry, Western blot, and qRT-PCR.
  • Assessment of key signaling molecules including PI3K, Akt, Bax, Bcl-2, Caspase-3, Caspase-9, mutant p53, TGF-β RI & RII, SMAD-2, SMAD-4, and SMAD-7.

Main Results:

  • Betanin (BTN) significantly attenuated OSCC progression in a dose-dependent manner.
  • BTN inhibited the expression of growth-regulatory proteins (PI3K, Akt, Bcl-2, mutant p53, TGF-β RI/RII, SMAD-2, SMAD-4).
  • BTN promoted the expression of pro-apoptotic proteins (SMAD-7, Bax, Caspase-3, Caspase-9), indicating enhanced apoptosis.

Conclusions:

  • Betanin (BTN) demonstrates multi-targeted anticancer potential in oral squamous cell carcinoma (OSCC).
  • BTN modulates key apoptotic and growth-regulatory signaling pathways, including PI3K/Akt and TGF-β.
  • These findings identify Betanin (BTN) as a potential chemopreventive agent for oral cancer, warranting further research.
Keywords:
ApoptosisBetaninChemopreventionOral cancerPhytochemical

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