MicroRNA-7 (miR-7) is a small non-coding RNA, which plays critical roles in regulating gene expression of multiple key cellular processes. MiR-7 exhibits a tissue-specific pattern of expression, with abundant levels found in the brain, spleen, and pancreas. Although it is expressed at lower levels in other tissues, including the liver, miR-7 is involved in both the development of organs and biological functions of cells. In this review, we focus on the mechanisms by which miR-7 controls cell growth, proliferation, invasion, metastasis, metabolism, and inflammation. We also summarize the specific roles of miR-7 in liver diseases. MiR-7 is considered as a tumor suppressor miRNA in hepatocellular carcinoma and is involved in the pathogenesis of hepatic steatosis and hepatitis. Future studies to further define miR-7 functions and its mechanism in association with other types of liver diseases should be explored. An improved understanding from these studies will provide us a useful perspective leading to mechanism-based intervention by targeting miR-7 for the treatment of liver diseases.
- liver diseases
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Contributors SH: literature review. SH, TZ and YJ: drafting the manuscript. PK, NH, SL and ZY: critical review of the manuscript. SH and SL: finalizing the manuscript. All authors have read and approved the manuscript for submission.
Funding ZY is supported by NIH K01AA26385, Indiana University Research Support Fund Grant (IU RSFG), the Ralph W. and Grace M. Showalter Research Trust Indiana University School of Medicine and Indiana Institute for Medical Research. SL is supported in part by R01 DK107682, R01 AA025208, U01 AA026917, UH2 AA026903, VA Merit Award 1I01CX000361 and Indiana Clinical and Translational Sciences Institute, UL1TR002529, National Center for Advancing Translational Sciences, Clinical and Translational Sciences Award and Showalter Scholar Indiana University School of Medicine. PK is supported by the grant from Indiana Institute for Medical Research (IIMR).
Competing interests None declared.
Patient consent for publication Not required.
Provenance and peer review Not commissioned; externally peer reviewed.
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