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<p>Pyrogallol, a polyphenolic compound, exhibits diverse activities, including antibacterial, antifungal, and antiviral effects; however, its anticancer potential has only been examined in a very few cancers and remains unexplored in T cell lymphoma. Hence, the present study is designed to elucidate the antitumor potential of pyrogallol against T cell lymphoma along with possible implication of modulated glucose metabolism and immune evasion. The experimental findings of this investigation show tumor-specific cytotoxicity of pyrogallol against T lymphoma cells. Further, pyrogallol has been shown to mediate G2/M cell cycle arrest by downregulating cyclin B1 and c-Myc expression, and induce apoptosis by altering ROS levels, mitochondrial membrane potential, and the expression of apoptosis regulators, namely Bcl2 and cleaved caspase 3, in T lymphoma cells. Furthermore, pyrogallol is observed to shift glucose metabolism towards oxidative phosphorylation by suppressing GLUT1, GLUT3, HKII, PKM2, PDK1, PDK3, and HIF-1α levels. Moreover, it suppresses the immune evasion ability of T lymphoma cells through deregulating ‘do not eat me’ and ‘find me’ signals, specifically PD-L1, CD-24 and CD-47, and S1P and LPC, respectively. Notably, the disrupted AKT pathway was found to play a critical role in pyrogallol-mediated T cell lymphoma growth inhibition. Overall, our investigation demonstrates that pyrogallol exerts tumor growth inhibitory effect in T lymphoma cells by modulating the cell cycle, apoptosis, glucose metabolism, and immune evasion in an AKT-dependent manner.</p>

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Pyrogallol inhibits T cell lymphoma growth by mediating G2/M phase cell cycle arrest, apoptosis, glycolysis and immune evasion: an implication of AKT pathway

  • 期刊论文

  • 发表日期：

    2026年7月17日

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  • Abhishek Kumar,
  • Mukesh Kumar,
  • Siddharth Rai,
  • Pratishtha Sonker,
  • Ajay Kumar

摘要

Pyrogallol, a polyphenolic compound, exhibits diverse activities, including antibacterial, antifungal, and antiviral effects; however, its anticancer potential has only been examined in a very few cancers and remains unexplored in T cell lymphoma. Hence, the present study is designed to elucidate the antitumor potential of pyrogallol against T cell lymphoma along with possible implication of modulated glucose metabolism and immune evasion. The experimental findings of this investigation show tumor-specific cytotoxicity of pyrogallol against T lymphoma cells. Further, pyrogallol has been shown to mediate G2/M cell cycle arrest by downregulating cyclin B1 and c-Myc expression, and induce apoptosis by altering ROS levels, mitochondrial membrane potential, and the expression of apoptosis regulators, namely Bcl2 and cleaved caspase 3, in T lymphoma cells. Furthermore, pyrogallol is observed to shift glucose metabolism towards oxidative phosphorylation by suppressing GLUT1, GLUT3, HKII, PKM2, PDK1, PDK3, and HIF-1α levels. Moreover, it suppresses the immune evasion ability of T lymphoma cells through deregulating ‘do not eat me’ and ‘find me’ signals, specifically PD-L1, CD-24 and CD-47, and S1P and LPC, respectively. Notably, the disrupted AKT pathway was found to play a critical role in pyrogallol-mediated T cell lymphoma growth inhibition. Overall, our investigation demonstrates that pyrogallol exerts tumor growth inhibitory effect in T lymphoma cells by modulating the cell cycle, apoptosis, glucose metabolism, and immune evasion in an AKT-dependent manner.