4.6 Article

Tannic Acid Exhibits Antiangiogenesis Activity in Nonsmall-Cell Lung Cancer Cells

Journal

ACS OMEGA
Volume 7, Issue 27, Pages 23939-23949

Publisher

AMER CHEMICAL SOC
DOI: 10.1021/acsomega.2c02727

Keywords

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Funding

  1. Department of Pharmaceutical Sciences, College of Pharmacy, University of Tennessee Health Science Center [SC1GM139727, R01 CA210192, R01 CA206069]
  2. Department of Pharmaceutical Sciences, College of Pharmacy, University of Tennessee Health Science Center
  3. Memphis and Department of Immunology and Microbiology, School of Medicine, University of Texas Rio Grande Valley
  4. National Institute of Health/National Cancer Institute [SC1GM139727, R01 CA210192, R01 CA206069]

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The study demonstrates that Tannic acid (TA) has antiproliferative and antiangiogenic effects against nonsmall-cell lung cancer (NSCLC).
Nonsmall-cell lung cancer (NSCLC) is the most common type of lung cancer, with a dismal prognosis. NSCLC is a highly vascularized tumor, and chemotherapy is often hampered by the development of angiogenesis. Therefore, suppression of angiogenesis is considered a potential treatment approach. Tannic acid (TA), a natural polyphenol, has been demonstrated to have anticancer properties in a variety of cancers; however, its angiogenic properties have yet to be studied. Hence, in the current study, we investigated the antiproliferative and antiangiogenic effects of TA on NSCLC cells. The (3-(4,5dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium) (MTS) assay revealed that TA induced a dose- and time-dependent decrease in the proliferation of A549 and H1299 cells. However, TA had no significant toxicity effects on human bronchial epithelial cells. Clonogenicity assay revealed that TA suppressed colony formation ability in NSCLC cells in a dose-dependent manner. The anti-invasiveness and antimigratory potential of TA were confirmed by Matrigel and Boyden chamber studies, respectively. Importantly, TA also decreased the ability of human umbilical vein endothelial cells (HUVEC) to form tube-like networks, demonstrating its antiangiogenic properties. Extracellular vascular endothelial growth factor (VEGF) release was reduced in TA-treated cells compared to that in control cells, as measured by the enzyme-linked immunosorbent assay (ELISA). Overall, these results demonstrate that TA can induce antiproliferative and antiangiogenic effects against NSCLC.

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