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Objective <p>This study investigated resveratrol impact on oral squamous cell carcinoma (OSCC) via the NORAD/IGF2BP2/PDK1 pathway.</p> Methods <p>CAL-27, SCC-25, and KB cell lines were used to evaluate cell proliferation, cell cycle arrest, and protein expression. Key molecular markers were assessed using Western blot, RNA interference, and functional assays.</p> Results <p>Resveratrol inhibited the growth of CAL-27, KB, and SCC-25 cancer cell lines in a dose-dependent manner, with IC50 values of 70, 145, and 125&#xa0;μg/mL, respectively (P &lt; 0.01). In CAL-27 cells, 50&#xa0;μg/mL resveratrol induced G2/M arrest (P &lt; 0.05); 100&#xa0;μg/mL caused S and G2/M phase arrest (P &lt; 0.01). Thirteen proteins changed significantly: cPKCα and Notch4 were upregulated, while p-ERK, p-PDK1, p-Cdc2, p-RB, NORAD, IGF2BP2, CDK2, Cdc2P34, Cyclin E, 14–3-3beta, and XIAP were downregulated. si-NORAD groups showed lower CAL-27 proliferation than control. IGF2BP2 silencing reduced proliferation to 69.13% in HSC3 and 74.01% in CAL-27 (P &lt; 0.001) and decreased invasion to 72.85% and 52.44% (P &lt; 0.001). PDK1 overexpression enhanced the proliferation and migration of hypopharyngeal cancer cells.</p> Conclusion <p>Resveratrol inhibits OSCC proliferation, particularly in CAL-27 cells. It affects NORAD, IGF2BP2, and PDK1 pathways, altering cell cycle protein expression and causing S and G2/M phase arrest.</p>

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Resveratrol inhibits the progression of oral squamouscell carcinoma through Norad/Igf2bp2/Pdk1 pathway and remodeling glucose metabolism reprogramming

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年4月24日

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  • Rongrong Zhang,
  • Jinjing Guo,
  • Yicong Lin

摘要

Objective

This study investigated resveratrol impact on oral squamous cell carcinoma (OSCC) via the NORAD/IGF2BP2/PDK1 pathway.

Methods

CAL-27, SCC-25, and KB cell lines were used to evaluate cell proliferation, cell cycle arrest, and protein expression. Key molecular markers were assessed using Western blot, RNA interference, and functional assays.

Results

Resveratrol inhibited the growth of CAL-27, KB, and SCC-25 cancer cell lines in a dose-dependent manner, with IC50 values of 70, 145, and 125 μg/mL, respectively (P < 0.01). In CAL-27 cells, 50 μg/mL resveratrol induced G2/M arrest (P < 0.05); 100 μg/mL caused S and G2/M phase arrest (P < 0.01). Thirteen proteins changed significantly: cPKCα and Notch4 were upregulated, while p-ERK, p-PDK1, p-Cdc2, p-RB, NORAD, IGF2BP2, CDK2, Cdc2P34, Cyclin E, 14–3-3beta, and XIAP were downregulated. si-NORAD groups showed lower CAL-27 proliferation than control. IGF2BP2 silencing reduced proliferation to 69.13% in HSC3 and 74.01% in CAL-27 (P < 0.001) and decreased invasion to 72.85% and 52.44% (P < 0.001). PDK1 overexpression enhanced the proliferation and migration of hypopharyngeal cancer cells.

Conclusion

Resveratrol inhibits OSCC proliferation, particularly in CAL-27 cells. It affects NORAD, IGF2BP2, and PDK1 pathways, altering cell cycle protein expression and causing S and G2/M phase arrest.