ArticleTranslational cancer research2026
PM2.5 promotes migration of hepatocellular carcinoma by targeting miR-25.
Article in Translational cancer research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Background: Studies have identified a correlation between fine particulate matter (PM2.5) exposure and the progression of hepatocellular carcinoma (HCC), though the underlying mechanisms remain unclear. This study investigates the regulatory effects of PM2.5 on HCC migration. Methods: Wound healing assays were conducted to evaluate the invasion and migration capabilities of liver cancer cells. Western blot and immunohistochemistry were employed to assess E-cadherin and Vimentin expression levels. Reverse transcription quantitative polymerase chain reaction (RT-qPCR) was used to measure miR-25 expression in both MHCC97H cells and liver cancer cells of mice. miR-25 mimics and inhibitors were transfected into MHCC97H cells to explore the role of miR-25 in PM2.5-induced progression of liver cancer cells. Results: PM2.5 exposure suppressed E-cadherin expression while upregulating Vimentin, thereby enhancing MHCC97H cell migration. PM2.5 also elevated miR-25 expression in MHCC97H cells. Transfection with miR-25 mimics further augmented PM2.5-induced migration, whereas transfection with miR-25 inhibitors attenuated these effects. This suggests that miR-25 serves as a key mediator in PM2.5-induced promotion of liver cancer invasion and migration. Animal experiments demonstrated that PM2.5 exposure facilitated tumor growth, invasion, and migration in liver cancer models, accompanied by elevated miR-25 expression levels. Conclusions: This study confirms that PM2.5 promotes HCC cell migration by targeting miR-25, and significantly promotes tumor growth and epithelial-mesenchymal transition (EMT) phenotypic alterations
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