4.7 Article

Apigenin suppresses tumor angiogenesis and growth via inhibiting HIF-1? expression in non-small cell lung carcinoma

期刊

CHEMICO-BIOLOGICAL INTERACTIONS
卷 361, 期 -, 页码 -

出版社

ELSEVIER IRELAND LTD
DOI: 10.1016/j.cbi.2022.109966

关键词

Non-small cell lung carcinoma; Angiogenesis inhibitor; Apigenin; HIF-1; Lung squamous carcinoma

资金

  1. National Key R&D Program of China [2021YFE0202000]
  2. National Natural Science Foundation of China [82104201]
  3. GuangDong Basic and Applied Basic Research Foundation [2019A1515110058]
  4. Medical Science and Technology Research Foun-dation of Guangdong Province [A2020289]
  5. High-level University Construction Fund of Guangdong Province [06-410-2107208]

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Apigenin not only inhibits the motility of tumor-related cells, but also reduces pericyte coverage. Further research shows that apigenin suppresses tumor angiogenesis by inhibiting HIF-1α and its downstream signaling pathways. In cell and animal models, apigenin exhibits a perfect anti-angiogenic effect and suppresses tumor growth. These findings suggest that apigenin may serve as a safe and effective angiogenesis inhibitor for NSCLC therapy.
Tumor angiogenesis inhibitors such as Bevacizumab, Ramucirumab and Endostar have been applied to the therapy of non-small cell lung carcinoma (NSCLC) patients, especially for lung adenocarcinoma (LUAD). However, several safe concerns such as neutropenia, febrile neutropenia and hypertension pulmonary hemorrhage limit their further development. And they often showed poor efficacy and serious side effect for lung squamous cell carcinoma (LUSC) patient. Thus, identification of effective and safe tumor angiogenesis inhibitor for NSCLC therapy is warranted. Apigenin is a bioflavonoid with potential anti-tumor effect and perfect safety, but its effect on tumor angiogenesis and underlying mechanism are still unclear. Herein, we found that apigenin not merely suppressed endothelial cells related motilities but also reduced pericyte coverage. Further research showed that apigenin had strong suppressive activity against HIF-1 alpha expression and its downstream VEGF-A/VEGFR2 and PDGF-BB/PDGF beta R signaling pathway. Apigenin also reduced microvessel density and pericyte coverage on the xengraft model of NCI-H1299 cells, leading to suppression of tumor growth. Moreover, apigenein showed perfect anti-angiogenic effect in xengraft model of LUSC cell NCI-H1703 cells, indicating it may be developed into a potential angiogenesis inhibitor for LUSC patient. Collectively, our study provides new insights into the antitumor mechanism of apigenin and suggests that apigenin is a safe and effective angiogenesis inhibitor for NSCLC therapy.

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