| Mechanism: | We Explored The Role Of Trf-5009A In The Posttranscriptional Gene Regulation Of Autophagy And Cartilage Degeneration In Oa. Using Rna Sequencing, We Identified Trf-5009A, The Trnavalcac-Derived Fragment, In Oa Tissues And Explored Its Expression By Quantitative Reverse Transcription Pcr And Fluorescence In Situ Hybridization. We Further Investigated The Relationship Between The Expression Of Trf-5009A And Clinical Factors In Oa. Chondrocytes Were Transfected With A Trf-5009A Inhibitor Or Mimic To Determine Their Functions, Including In Relation To Autophagy And The Cartilage Phenotype. A Rescue Experiment And Dual-Luciferase Reporter Assay Were Conducted To Determine Whether The 3'-Untranslated Region (Utr) Of Mtor Contains A Trf-5009A-Binding Site. Trf-5009A Was Downregulated In The Cartilage Of Oa Knees, Especially In Damaged Areas. Mtor Was Highly Expressed In Damaged Cartilage And Negatively Correlated With The Expression Of Trf-5009A; Transfection With A Trf-5009A Inhibitor Promoted The Expression Of Mtor And Suppressed Autophagy, Whereas Transfection With A Trf-5009A Mimic Had The Opposite Effect. A Dual-Luciferase Reporter Assay Showed That Trf-5009A Silenced The Expression Of Mtor By Binding To Its 3'-Utr. Thus, Trf-5009A Regulates Autophagy And Cartilage Degeneration In Oa By Targeting Mtor. In Summary, These Findings Provide An Additional Tool For The Clinical Diagnosis And Novel Targeted Therapy Of Oa. |