miR-361-3p Regulates Liver Tumor-initiating Cells Expansion and Chemo-resistance

Increasing evidence shows that liver tumor-initiating cells (T-ICs) closely associated with the progression, metastasis, recurrence and chemo-resistance of hepatocellular carcinoma (HCC). However, the underlying mechanism for the propagation of liver T-ICs remains unclear. Here we show that miR-361-...

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Bibliographic Details
Published in:Journal of Cancer 2021, Vol.12 (5), p.1483-1492
Main Authors: Qu, Shuping, Zhang, Xiaobing, Wu, Yue, Li, HengYu, Zhai, Jian, Wu, Dong
Format: Article
Language:English
Subjects:
Apoptosis
Binding sites
Breast cancer
Flow cytometry
Liver cancer
MicroRNAs
Research Paper
Spheroids
Statistical analysis
Surgery
Tumorigenesis
Tumors
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Summary:Increasing evidence shows that liver tumor-initiating cells (T-ICs) closely associated with the progression, metastasis, recurrence and chemo-resistance of hepatocellular carcinoma (HCC). However, the underlying mechanism for the propagation of liver T-ICs remains unclear. Here we show that miR-361-3p is upregulated in liver T-ICs. Knockdown of miR-361-3p impairs the self-renewal and tumorigenicity liver T-ICs. Conversely, forced miR-361-3p expression enhances the self-renewal and tumorigenicity liver T-ICs. Mechanistically, miR-361-3p directly targets SOX1 via binding its 3'-UTR in liver T-ICs. Moreover, miR-361-3p knockdown hepatoma cells are more sensitive to cisplatin or sorafenib treatment. Clinical cohort analysis demonstrates that miR-361-3p low HCC patients are benefited from TACE (transcatheter arterial chemoembolization) or sorafenib treatment. In conclusion, our findings revealed the crucial role of the miR-361-3p in liver T-IC expansion and TACE or sorafenib response, rendering miR-361-3p an optimal target for the prevention and intervention in HCC.
ISSN:1837-9664
1837-9664
DOI:10.7150/jca.52395