Translational cancer research · 2026
PM2.5 promotes migration of hepatocellular carcinoma by targeting miR-25.
СтатьяНазвание и аннотация: Перевод пока не подготовлен
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Li Qiaoxin, Lu Yuxuan, Guo Quanyu, Jin Tianle, Lu Le, Shang Hao, Fan Meng, Mo Jiantao, Zhang Hua, Feng Wanying, Da Xuanbo, Lu Hongwei
Аннотация
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 in vivo, indicating that PM2.5 exposure drives HCC malignant progression through miR-25 dysregulation. Importantly, it also provides the first direct functional link among PM2.5 exposure, miR-25 dysregulation, and HCC progression, and identify miR-25 as a potential therapeutic target and prognostic biomarker for HCC.
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 in vivo, indicating that PM2.5 exposure drives HCC malignant progression through miR-25 dysregulation. Importantly, it also provides the first direct functional link among PM2.5 exposure, miR-25 dysregulation, and HCC progression, and identify miR-25 as a potential therapeutic target and prognostic biomarker for HCC.