摘要Posterior capsule opacification (PCO) results from the proliferation,migration,and epithelialmesenchymal transition (EMT) of residual lens epithelial cells (LECs) and fibers in the capsular bag.Previous reports have demonstrated that transforming growth factor β2 (TGF-β2) affects the cellular processes via modulation of EMT in LECs.However,the mechanisms that underlie the TGF-β2 induced EMT in LECs are still largely unknown.In this study,we confirmed that TGF-β2 induces EMT in SRA01/04 cells via the up-regulation of the long non-coding RNA (IncRNA) HOTAIR.To study the effects of HOTAIR on the proliferation,migration and EMT of SRA01/04 cells as well as the underlying mechanism,we used small interfering RNA (siRNA) to specifically attenuate HOTAIR expression in SRA01/04 cells.CCK8 cell-counting kit was used to examine SRA01/04 cell viability;EdU cell proliferation kit was used to examine SRA01/04 cell proliferation;Transwell system and scratch assays were used to observe cell migration;and qPCR and western blot analysis were used to evaluate EMT progression.We found that inhibition of HOTAIR expression repressed SRA01/04 cell viability,proliferation,migration and prevented the TGF-β2-induced changes in cellular processes via modulation of EMT.Ultimately,we found that HOTAIR affected the TGF-β/ Smad signaling pathway.In summary,we elucidated that HOTAIR affected the cell viability,prolif eration,and migration in the TGF-β2-induced EMT in SRA01/04 cells and suggested that modulation of HOTAIR may be helpful in PCO prevention and therapy.