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Cancer cells corrupt normal epithelial cells through miR-let-7c-rich small extracellular vesicle-mediated downregulation of p53/PTEN

引用

International Journal of Oral Science 2022年第4期14卷 470-478页

作者： Weilian Liang Yang Chen Hanzhe Liu Hui Zhao Tingting Luo hokeung tang Xiaocheng Zhou Erhui Jiang Zhe Shao Ke Liu Zhengjun Shang The State Key Laboratory Breeding Base of Basic Science of Stomatology(Hubei-MOST)&Key Laboratory for Oral Biomedicine Ministry of Education School and Hospital of StomatologyWuhan UniversityWuhanChina Shenzhen PKU-HKUST Medical Center(Peking University Shenzhen Hospital) ShenzhenChina Department of Oral and Maxillofacial Surgery School and Hospital of StomatologyWuhan UniversityWuhanChina Department of Oral and Maxillofacial-Head and Neck oncology School&Hospital of StomatologyWuhan UniversityWuhanChina

Tumor volume increases continuously in the advanced stage, and aside from the self-renewal of tumor cells, whether the oncogenic transformation of surrounding normal cells is involved in this process is currently unclear. Here, we show that oral squamous cell carcinoma(OSCC)-derived small extracellular vesicles(s EVs) promote the proliferation, migration, invasion, and epithelial-mesenchymal transition(EMT) of normal epithelial cells but delay their apoptosis. In addition, nuclear-cytoplasmic invaginations and multiple nucleoli are observed in s EV-treated normal cells, both of which are typical characteristics of premalignant lesions of OSCC. Mechanistically, mi Rlet-7c in OSCC-derived s EVs is transferred to normal epithelial cells, leading to the transcriptional inhibition of p53 and inactivation of the p53/PTEN pathway. In summary, we demonstrate that OSCC-derived s EVs promote the precancerous transformation of normal epithelial cells, in which the mi R-let-7c/p53/PTEN pathway plays an important role. Our findings reveal that cancer cells can corrupt normal epithelial cells through s EVs, which provides new insight into the progression of OSCC.

关键词： cor invasion transferred

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