期刊
ARCHIVES OF BIOCHEMISTRY AND BIOPHYSICS
卷 703, 期 -, 页码 -出版社
ELSEVIER SCIENCE INC
DOI: 10.1016/j.abb.2021.108871
关键词
Hepatocellular carcinoma; Tumor initiating cells; miR-93; MTMR3
资金
- Project of Shanghai Science and Technology Commission [1914220700]
MiR-93 is highly expressed in liver T-ICs, enhancing their self-renewal and tumorigenesis abilities by regulating MTMR3 and contributing to drug resistance. Patients with low miR-93 levels benefit more from TACE or sorafenib treatment in HCC cases.
Tumor initiating cells (T-ICs) play an important role in tumorigenesis, progression, metastasis, recurrence and drug resistance, but the underlying mechanism was not clearly elucidated. In our study, we found that miR-93 was highly expressed in liver T-ICs. Self-renewal and tumorigenesis ability of liver T-ICs were enhanced by miR93 overexpression and attenuated by miR-93 interference. Mechanically, miR-93 regulated liver T-ICs by binding to 3?-UTR of myotubularin-related protein 3 (MTMR3). In addition, miR-93 was found highly expressed in cisplatin or sorafenib-resistant liver cancer tissues. Interference of miR-93 sensitizes hepatoma cells to cisplatin or sorafenib treatment. Clinical cohort analysis showed that Hepatocellular carcinoma (HCC) patients with low miR-93 were benefit more from TACE or sorafenib treatment. In conclusion, our study demonstrates a new regulation mechanism of liver T-ICs, a new target for HCC, and a biomarker for postoperative TACE or sorafenib.
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