LncRNA HOTAIR mediates TGF-ß2-induced cell growth and epithelial-mesenchymal transition in human lens epithelial cells.

ABSTRACT

Posterior capsule opacification (PCO) results from the proliferation, migration, and epithelial-mesenchymal transition (EMT) of residual lens epithelial cells (LECs) and fibers in the capsular bag. Previous reports have demonstrated that transforming growth factor ß2 (TGF-ß2) affects the cellular processes via modulation of EMT in LECs. However, the mechanisms that underlie the TGF-ß2-induced EMT in LECs are still largely unknown. In this study, we confirmed that TGF-ß2 induces EMT in SRA01/04 cells via the up-regulation of the long non-coding RNA (lncRNA) 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-ß2-induced changes in cellular processes via modulation of EMT. Ultimately, we found that HOTAIR affected the TGF-ß/Smad signaling pathway. In summary, we elucidated that HOTAIR affected the cell viability, proliferation, and migration in the TGF-ß2-induced EMT in SRA01/04 cells and suggested that modulation of HOTAIR may be helpful in PCO prevention and therapy.