Introduction Long intergenic non‐protein coding RNA 1138 (LINC01138) plays a vital role in human cancers. In this study, we aimed to investigate the effect of LINC01138 on the progression of osteoarthritis (OA) and explore its potential mechanism of action. Methods The expression of LINC01138, hsa‐miR‐1207‐5p, and KIAA0101 in OA tissues and normal tissues was analyzed using GSEA datasets and confirmed in human specimens. Human chondrocytes were treated with interleukin (IL)‐1β to establish an OA cell model. Quantitative real time PCR(qRT‐PCR), enzyme‐linked immunosorbent assay, and western blotting analyses were performed to evaluate the role of LINC01138, hsa‐miR‐1207‐5p, and KIAA0101 during extracellular matrix (ECM) protein degeneration and cellular inflammatory response. The target relationship was predicted using DIANA‐TarBase and TargetScan. The binding effects were verified by dual‐luciferase reporter assay. Results LINC01138 expression was higher in OA tissues than in normal controls. LINC01138 levels increased in chondrocytes treated with IL‐1β. Silencing of LINC01138 attenuated the IL‐1β‐induced decrease in Col2α1, aggrecan, and sulphated glycosaminoglycan (sGAG), and inhibited the IL‐1β‐induced increase in matrix metalloproteinase (MMP)‐13, IL‐6, and tumor necrosis factor (TNF)‐α. miR‐1207‐5p is weakly expressed in OA tissues and cell models. The inhibition of hsa‐miR‐1207‐5p, a target of LINC01138, attenuated the effects of LINC01138 silencing on chondrocyte ECM degeneration and inflammatory responses. Silencing KIAA0101, a target of hsa‐miR‐1207‐5p, alleviated the effect of hsa‐miR‐1207‐5p on chondrocyte ECM degeneration and inflammatory responses. Furthermore, silencing of KIAA0101 inhibited the JAK/STAT and Wnt signaling pathways. Conclusion Silencing LINC01138 protected chondrocytes from IL‐1β‐induced damage, possibly by regulating the hsa‐miR‐1207‐5p/KIAA0101 axis.