Long non-coding RNA HOTAIRM1-1 silencing in cartilage tissue induces osteoarthritis through microRNA-125b

xlomafota13 shared this article with you from Inoreader Long non-coding RNA HOTAIRM1-1 silencing in cartilage tissue induces osteoarthritis through microRNA-125b Via Experimental and therapeutic medicine Exp Ther Med. 2021 Sep;22(3):933. doi: 10.3892/etm.2021.10365. Epub 2021 Jul 1. ABSTRACT Aberrations in long noncoding RNA (lncRNA) expression have been recognized in numerous human diseases. In the present study, the of role the long noncoding RNA HOX antisense intergenic RNA myeloid 1 variant (HOTAIRM1-1) in regulating the pathological progression of osteoarthritis (OA) was investigated. The aberrant expression of HOTAIRM1-1 in OA was demonstrated, but the molecular mechanisms require further analysis. The aim of the present study was to explore the function of miR-125b in modulating chondrocyte viability and apoptosis, and to address the functional association between HOTAIRM1-1 and miR-125b as potential targets. A miR-125b inhibitor was used, which laid the foundation for the following investigation. The study confirmed that HOTAIRM1-1 and miR-125b are inversely expressed in chondrocytes. The expression of HOTAIRM1-1 was downregula ted and the expression of miR-125b was upregulated in tissues from patients with OA. HOTAIRM1-1 directly interacted with miR-125b in chondrocytes. HOTAIRM1-1 knockdown was associated with chondrocyte proliferation and extracellular matrix degradation. Furthermore, miR-125b reversed the effect of HOTAIRM1-1 on cell proliferation and apoptosis. In conclusion, the present study indicates that the loss of HOTAIRM1-1 function leads to aberrant increases in the proliferation and apoptosis of chondrocytes. miR-125b may be a potential downstream mechanism that regulates the function of HOTAIRM1-1, and this finding provides a therapeutic strategy for OA. PMID:34306202 | PMC:PMC8280714 | DOI:10.3892/etm.2021.10365 View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.