ArticleThe Kaohsiung journal of medical sciences2020
MicroRNA-216b suppresses the cell growth of hepatocellular carcinoma by inhibiting Ubiquitin-specific peptidase 28 expression.
Article in The Kaohsiung journal of medical sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 11 citations in OpenAlex.
- Targeting the deubiquitinase USP28 in cancer: navigating context-dependent mechanisms and therapeutic resistance.Frontiers in immunology · 2026Review
- Deubiquitinase USP28 promotes the malignant progression and radio-resistance of hepatocellular carcinoma by stabilizing WDHD1.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- Deubiquitylating Enzymes in Hepatocellular Carcinoma.International journal of biological sciences · 2025Review
- Resveratrol inhibits Lin28A expression and induces its degradation via the proteasomal pathway in NCCIT cells.Oncology letters · 2024Article
- Deubiquitinating enzyme USP28 inhibitor AZ1 alone and in combination with cisplatin for the treatment of non-small cell lung cancer.Apoptosis : an international journal on programmed cell death · 2024Article
- Ubiquitin-specific protease 28: the decipherment of its dual roles in cancer development.Experimental hematology & oncology · 2023Review
- Review
- MicroRNA-216b suppresses the cell growth of hepatocellular carcinoma by inhibiting Ubiquitin-specific peptidase 28 expression.The Kaohsiung journal of medical sciences · 2020Article
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1 author at 1 institution in 1 country.
Funding
Abstract
MicroRNA-216b (miR-216b) has been reported to be downregulated in several tumors, its mechanism is still little-studied in hepatocellular carcinoma (HCC). In the present study, we found that miR-216b was downregulated in HCC, but Ubiquitin-specific peptidase 28 (USP28) was upregulated. In addition, Kaplan-Meier-plotter analysis indicated that liver cancer patients with high miR-216b expression had a longer overall survival, but patients with high USP28 had a shorter overall survival. Further studies showed that overexpression of miR-216b inhibited HCC cell growth, and molecular investigations revealed that miR-216b targeted USP28 and inhibited its expression in HCC cells. In addition, overexpression of miR-216b suppressed the substrates' expression of USP28, for example, c-Myc, and miR-216b overexpression also inhibited Cyclin E expression as well as upregulating p27 expression, both of which were the downstream signals of c-Myc. These results indicated that miR-216b downregulated USP28/c-Myc signaling in HCC cells. Collectively, this study demonstrated that miR-216b/c-Myc axis could be as a potential target for HCC therapy in the future.
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Registered trials
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