ArticleBioengineered2021
Long non-coding RNA HOTAIRincreased mechanical stimulation-induced apoptosis by regulating microRNA-221/BBC3 axis in C28/I2 cells.
Article in Bioengineered, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 8 citations in OpenAlex.
- Expression Profiles of Long Non-Coding RNAs in the Articular Cartilage of Rats Exposed to T-2 Toxin.International journal of molecular sciences · 2023Article
- Naringenin induces the cell apoptosis of acute myeloid leukemia cells by regulating the lncRNA XIST/miR-34a/HDAC1 signaling.Heliyon · 2023Article
- The emerging role of lncRNAs in osteoarthritis development and potential therapy.Frontiers in genetics · 2023Review
- Histone demethylase JMJD3 downregulation protects against aberrant force-induced osteoarthritis through epigenetic control of NR4A1.International journal of oral science · 2022Article
- MiR-20a-5p facilitates cartilage repair in osteoarthritis via suppressing mitogen-activated protein kinase kinase kinase 2.Bioengineered · 2022Article
- Emerging role of lncRNAs in osteoarthritis: An updated review.Frontiers in immunology · 2022Review
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
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Abstract
Abnormal mechanical stimulation contributes to articular cartilage degeneration and osteoarthritis (OA) development. Many long noncoding RNAs (lncRNAs) are involved in mechanical force-induced cartilage degeneration. LncRNA HOTAIR (HOTAIR) has been demonstrated to increase osteoarthritis progression. However, the roles of HOTAIR in mechanical stimulation-treated chondrocytes are still unclear. In this study, we found that mechanical stimulation significantly induced apoptosis in C28/I2 cells. In addition, the expression of HOTAIR was up regulated and the expression of miR-221 was down regulated. Knockdown of HOTAIR effectively ameliorated cell apoptosis induced by mechanical stimulation. HOTAIR could interact with miR-221, which targeted to degrade BBC3. Overexpression of BBC3 could reverse the decreased apoptotic rates induced by HOTAIR knockdown. Collectively, HOTAIR promoted mechanical stimulation-induced apoptosis by regulating the miR-221/BBC3 axis in C28/I2 cells.
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