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<p>High-risk human papillomavirus (HPV), especially HPV16 and HPV18, are closely linked to the onset of cervical cancer (CC). Astragalin (AST), a bioactive flavonoid, has been reported to impede CC HeLa cell proliferation. Nevertheless, the mechanism by which AST exerts its tumor-suppressive role in CC remains unclear. HeLa (HPV18-positive) and CaSki (HPV16-positive) cells were exposed to various concentrations of AST. CCK-8 assay, flow cytometry analysis, wound healing, and Transwell assays were employed to examine the AST functions on CC cell aggressiveness. Protein levels were assessed by western blotting. Immunofluorescence staining was used to detect E6, E7, p53, and p-pRb expression. Animal experiments were performed to validate the anti-CC role in vivo. The results showed that&#xa0;AST dose-dependently impaired HeLa and CaSki cell viability and elicited G1 cell cycle arrest. AST restrained CC cell migration and invasiveness. AST inhibited the growth of HeLa-derived xenograft tumors in mice and repressed E6/E7 oncoprotein expression in CC cells and mouse tumor tissues. In conclusion,&#xa0;AST suppresses CC progression by downregulating E6/E7 oncoprotein expression to attenuate CC cell aggressiveness.</p>

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Astragalin inhibits the proliferation of high-risk HPV-positive cervical epithelial cells and attenuates malignant cervical lesions

  • 期刊论文

  • 发表日期：

    2025年3月19日

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  • Wei Zeng,
  • Li Chen

摘要

High-risk human papillomavirus (HPV), especially HPV16 and HPV18, are closely linked to the onset of cervical cancer (CC). Astragalin (AST), a bioactive flavonoid, has been reported to impede CC HeLa cell proliferation. Nevertheless, the mechanism by which AST exerts its tumor-suppressive role in CC remains unclear. HeLa (HPV18-positive) and CaSki (HPV16-positive) cells were exposed to various concentrations of AST. CCK-8 assay, flow cytometry analysis, wound healing, and Transwell assays were employed to examine the AST functions on CC cell aggressiveness. Protein levels were assessed by western blotting. Immunofluorescence staining was used to detect E6, E7, p53, and p-pRb expression. Animal experiments were performed to validate the anti-CC role in vivo. The results showed that AST dose-dependently impaired HeLa and CaSki cell viability and elicited G1 cell cycle arrest. AST restrained CC cell migration and invasiveness. AST inhibited the growth of HeLa-derived xenograft tumors in mice and repressed E6/E7 oncoprotein expression in CC cells and mouse tumor tissues. In conclusion, AST suppresses CC progression by downregulating E6/E7 oncoprotein expression to attenuate CC cell aggressiveness.