Abstract：Objective: To investigate the impact of long non-coding RNA (LncRNA) metastasis associated lung adenocarcinoma transcript 1 (MALAT1) on interleukin-1β (IL-1β) -induced chondrocyte injury, and to determine whether it is related to microRNA-106a-5p (miR-106a-5p)/mother against decapentaplegic homolog 7 (Smad7). Methods: The human chondrocyte line C20/A4 was used as the research subject, and a chondrocyte injury model was induced by IL-1β. The cells were assigned into IL-1β group, IL-1β+sh-NC group, IL-1β+sh-MALAT1 group, IL-1β+sh-MALAT1+inhibitor NC group, and IL-1β+sh-MALAT1+miR-106a-5p inhibitor group. The control group was C20/A4 without IL-1β induction. QRT-PCR was performed to detect the mRNA expression of LncRNA MALAT1, miR-106a-5p, and Smad7. MTT and flow cytometry were performed to detect cell proliferation and apoptosis. ELISA was performed to detect IL-6, IL-8, and IL-10. Dual luciferase reporter assay was used to validate the targeting relationship between miR-106a-5p with LncRNA MALAT1 and Smad7. In addition, Western blot was used to detect apoptosis related proteins. Results: Compared with the control group, the IL-1β group showed increased LncRNA MALAT1, Smad7 mRNA expression, cell proliferation inhibition rate, apoptosis rate, IL-6, IL-8 levels, and Bax protein expression, and decreased miR-106a-5p expression, IL-10 level, and Bcl-2 protein expression (P<0.05). Compared with the IL-1β group and the IL-1β+sh-NC group, the IL-1β+sh-MALAT1 group had reduction in LncRNA MALAT1, Smad7 mRNA expression, cell proliferation inhibition rate, apoptosis rate, IL-6, IL-8 levels, and Bax protein expression, and elevation in miR-106a-5p expression, IL-10 level, and Bcl-2 protein expression (P<0.05). Compared with the IL-1β+sh-MALAT1 group and the IL-1β+sh-MALAT1+inhibitor NC group, the IL-1β+sh-MALAT1+miR-106a-5p inhibitor group showed no significant difference in LncRNA MALAT1 expression (P>0.05), reduced miR-106a-5p expression, IL-10 level, and Bcl-2 protein expression, and elevated Smad7 mRNA expression, cell proliferation inhibition rate, apoptosis rate, IL-6, IL-8 levels, and Bax protein expression (P<0.05). MALAT1 targeted the regulation of miR-106a-5p/Smad7 axis. Conclusion: Silencing MALAT1 can upregulate miR-106a-5p and inhibit Smad7, thereby promoting cell proliferation, inhibiting cell apoptosis and inflammatory response, and alleviating IL-1β - induced chondrocyte injury.
白波, 马佳良, 刘永权, 张玉舰, 陈国栋. LncRNA MALAT1靶向miR-106a-5p/Smad7对IL-1β诱导的软骨细胞损伤的影响[J]. 河北医学, 2025, 31(7): 1102-1109.
BAI Bo, MA Jialiang, LIU Yongquan, et al. Impact of LncRNA MALAT1 on IL-1β-Induced Chondrocyte Injury by Targeting miR-106a-5p/Smad7. HeBei Med, 2025, 31(7): 1102-1109.
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2025, Vol. 31 
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