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<p>This study explores the antitumor effect of tannic acid (TA), a natural polyphenol derived from gallnuts, on lung adenocarcinoma (LUAD), with a focus on its impact on epithelial-mesenchymal transition (EMT) and matrix metalloproteinase-2 (MMP-2). We employed CCK-8, wound healing, and Transwell assays to assess the effects of TA on the malignant behaviors of A549 LUAD cells. Western blot (WB) and immunofluorescence were used to examine EMT-related protein expression. Molecular docking was used to analyze TA-MMP-2 binding interaction. RT-qPCR, WB, and MMP-2 activity assay were applied to evaluate the expression and enzymatic activity of MMP-2. An MMP-2-overexpressing cell model was established to clarify its role in TA-mediated antitumor activity. Furthermore, an A549 subcutaneous xenograft model was employed to verify the in vivo antitumor efficacy of TA and its impact on MMP-2. TA markedly suppressed the viability, migration, and invasion of LUAD cells, downregulated the EMT-associated transcription factors Twist and Snail, downregulated N-cadherin and vimentin, and upregulated E-cadherin. Molecular docking indicated stable binding of TA to MMP-2 via multiple hydrogen bonds. TA downregulated MMP-2 at both mRNA and protein levels and suppressed its enzymatic activity. Overexpression of MMP-2 partially reversed the inhibitory effects of TA on cell viability, migration, invasion, and EMT. In vivo, TA markedly suppressed tumor growth, reduced MMP-2 expression, and inhibited EMT, whereas MMP-2 overexpression attenuated these antitumor effects. In conclusion, TA suppresses LUAD progression by inhibiting MMP-2 expression and activity, thereby interfering with the EMT process. MMP-2 is a key target of TA, suggesting its potential as a therapeutic agent.</p> Graphical Abstracts <p>Tannic acid (TA) markedly suppresses cell viability, migration, invasion, and tumor growth of lung adenocarcinoma A549 cells. Mechanistically, TA inhibits epithelial–mesenchymal transition (EMT) by targeting and downregulating MMP-2 expression. This effect is characterized by upregulation of the epithelial marker E-cadherin, accompanied by downregulation of the mesenchymal markers N-cadherin and vimentin, as well as the EMT-related transcription factors Twist and Snail.</p> <p></p>

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Tannic Acid Inhibits Lung Adenocarcinoma Progression by Suppressing MMP-2-Mediated Epithelial-Mesenchymal Transition

  • 期刊论文

  • 发表日期：

    2026年3月25日

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  • Min Lin,
  • Yu Zhou,
  • Yizhi Wang,
  • Huachun Yan,
  • Xuejun Qin,
  • Xiao Zhong,
  • Guozhong Yang,
  • Qi Liu

摘要

This study explores the antitumor effect of tannic acid (TA), a natural polyphenol derived from gallnuts, on lung adenocarcinoma (LUAD), with a focus on its impact on epithelial-mesenchymal transition (EMT) and matrix metalloproteinase-2 (MMP-2). We employed CCK-8, wound healing, and Transwell assays to assess the effects of TA on the malignant behaviors of A549 LUAD cells. Western blot (WB) and immunofluorescence were used to examine EMT-related protein expression. Molecular docking was used to analyze TA-MMP-2 binding interaction. RT-qPCR, WB, and MMP-2 activity assay were applied to evaluate the expression and enzymatic activity of MMP-2. An MMP-2-overexpressing cell model was established to clarify its role in TA-mediated antitumor activity. Furthermore, an A549 subcutaneous xenograft model was employed to verify the in vivo antitumor efficacy of TA and its impact on MMP-2. TA markedly suppressed the viability, migration, and invasion of LUAD cells, downregulated the EMT-associated transcription factors Twist and Snail, downregulated N-cadherin and vimentin, and upregulated E-cadherin. Molecular docking indicated stable binding of TA to MMP-2 via multiple hydrogen bonds. TA downregulated MMP-2 at both mRNA and protein levels and suppressed its enzymatic activity. Overexpression of MMP-2 partially reversed the inhibitory effects of TA on cell viability, migration, invasion, and EMT. In vivo, TA markedly suppressed tumor growth, reduced MMP-2 expression, and inhibited EMT, whereas MMP-2 overexpression attenuated these antitumor effects. In conclusion, TA suppresses LUAD progression by inhibiting MMP-2 expression and activity, thereby interfering with the EMT process. MMP-2 is a key target of TA, suggesting its potential as a therapeutic agent.

Graphical Abstracts

Tannic acid (TA) markedly suppresses cell viability, migration, invasion, and tumor growth of lung adenocarcinoma A549 cells. Mechanistically, TA inhibits epithelial–mesenchymal transition (EMT) by targeting and downregulating MMP-2 expression. This effect is characterized by upregulation of the epithelial marker E-cadherin, accompanied by downregulation of the mesenchymal markers N-cadherin and vimentin, as well as the EMT-related transcription factors Twist and Snail.