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Downregulation of miR-451 in cholangiocarcinoma help the diagnsosi and promotes tumor progression

BACKGROUND: Cholangiocarcinoma is a kind of invasive malignant tumor followed by hepatocellular carcinoma. miR-451 was suggested to function as regulator in various human tumors, but its role in mediating tumor progression and predicting the prognosis of cholangiocarcinoma remains unknown. The clini...

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Detalles Bibliográficos
Autores principales: Guo, Dengfang, Wang, Qingling, Huang, Jiancheng, Hu, Zhanglin, Chen, Chun, Zhang, Chun, Lin, Feng
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9647969/
https://www.ncbi.nlm.nih.gov/pubmed/36352360
http://dx.doi.org/10.1186/s12860-022-00445-2
Descripción
Sumario:BACKGROUND: Cholangiocarcinoma is a kind of invasive malignant tumor followed by hepatocellular carcinoma. miR-451 was suggested to function as regulator in various human tumors, but its role in mediating tumor progression and predicting the prognosis of cholangiocarcinoma remains unknown. The clinical significance and biological function of miR-451 in cholangiocarcinoma were assessed in this study. RESULTS: The tissue and serum expression of miR-451 was decreased in cholangiocarcinoma compared with corresponding normal samples. The downregulation of miR-451 was associated with the progressive TNM stage and positive lymph node metastasis of patients. miR-451 was identified to be an indicator of the diagnosis and prognosis of cholangiocarcinoma distinguishing cholangiocarcinoma patients from healthy volunteers and predicting the poor outcome of patients. miR-451 also served as a tumor suppressor negatively regulating the cellular processes of cholangiocarcinoma. CONCLUSIONS: miR-451 played a vital role in the early detection and risk prediction of cholangiocarcinoma. miR-451 also suppressed the progression of cholangiocarcinoma, which provides a potential therapeutical target for cholangiocarcinoma treatment. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s12860-022-00445-2.