Rheumatoid arthritis (RA) is an inflammatory and autoimmune disease that affects ~1% of the world's population. Although the precise mechanism of RA has yet to be elucidated, accumulating evidence suggests that fibroblast‑like synoviocytes (FLSs) serve critical roles in the initiation and progression of RA. However, the underlying molecular mechanisms of FLS proliferation have yet to be elucidated. Long noncoding‑interleukin‑7 receptor (lnc‑IL7R) has been recently identified, which is activated by lipopolysaccharide (LPS) stimulation and diminishes the LPS‑induced inflammatory response. In the present study, gain‑ and loss‑of‑function assays were performed in order to investigate the role of lnc‑IL7R in FLS. It is demonstrated, to the best of the authors' knowledge for the first time, that lnc‑IL7R promotes cell proliferation, cell cycle progression and inhibits apoptosis in FLS. Further investigation identified that lnc‑IL7 interacts with enhancer of zeste homolog 2 (EZH2) and is required for polycomb repressive complex 2 (PRC2)‑mediated suppression, including cyclin‑dependent kinase inhibitor 1A and cyclin‑dependent kinase inhibitor 2A. Lnc‑IL7R may be a promising therapeutic target for the treatment of RA.