lncRNA MALAT1 promotes chondrocyte proliferation by inhibiting MiR-127-5p

Objective: To investigate the effect of MALAT1 on the biological function of chondrocytes and its molecular mechanism. Methods: One hundred and two patients with osteoarthritis surgery in Ningbo No. 6 Hospital were selected as the research group (RG), and 69 patients with femoral neck fracture surgery were enrolled as the control group (CG). The cartilage tissue culture cells were removed, and PCR analysis was performed to measure the expression levels of MALAT and miR-127-5p in the serum and chondrocyte cell lines of the two groups of patients. The correlation between serum MALAT expression and clinical pathological features and prognosis in patients with osteoarthritis was analyzed. In addition, the biological function of MALAT on osteoarthritis chondrocytes was determined in vitro, and the regulatory relationship between MALAT and miR-127-5p in osteoarthritis was explored. Results: MALAT was highly expressed in the serum of patients with osteoarthritis, while miR-127-5p was lowly expressed, with a negative correlation between the two. Through Cox analysis, it was found that high expression of MALAT1, age, housework, family history of osteoarthritis, history of knee trauma, damp and dark living environment and obesity were independent factors affecting the prognosis of patients with osteoarthritis. Overexpression of miR-127-5p silenced MALAT1 to inhibit the proliferation and invasion of osteoarthritis chondrocytes, but increased the rate of apoptosis. After co-transfection with MALAT1-inhibitor+miR-127-5p-mimc, the proliferation and invasion of chondrocytes were markedly inhibited, and the apoptosis rate was clearly increased. Inhibition of MALAT1 could improve the expression of miR-127-5p, thereby reducing the proliferation and invasion ability of chondrocytes in osteoarthritis, but significantly increasing the rate of apoptosis. Conclusion: MALAT1 promoted osteoarthritis chondrocyte proliferation and prevented apoptosis by targeting miR-127-5p.