LncRNA FEZF1-AS1 Promotes TGF-β2-Mediated Proliferation and Migration in Human Lens Epithelial Cells SRA01/04

Abstract

Posterior capsule opacification (PCO) is a common complication after cataract surgery attributed to the proliferation and migration of postoperative residual lens epithelial cells (LECs). The long noncoding RNA (lncRNA) FEZ family zinc finger 1 antisense RNA 1 (FEZF1-AS1) promotes the proliferation and migration of multiple types of cancer cells. Here, we discovered that FEZF1-AS1 is markedly upregulated in TGF-β2-treated SRA01/04 cells. In addition, the proliferation and migration of SRA01/04 cells were enhanced following TGF-β2 treatment. FEZF1-AS1 knockdown inhibited the TGF-β2-induced proliferation and migration of SRA01/04 cells. Accordingly, FEZF1-AS1 overexpression promoted the TGF-β2-induced proliferation and migration of SRA01/04 cells. Finally, FEZF1-AS1 upregulated TGF-β2-induced SRA01/04 cell proliferation and migration via boosting FEZF1 protein levels. Our findings indicate that the dysregulation of FEZF1-AS1 participates in the TGF-β2-induced proliferation and migration of human lens epithelial cells (HLECs), which might be achieved, at least in part, through the induction of FEZF1 expression.

Knockdown of lncRNA XIST prevents the epithelial-mesenchymal transition of TGF-β2-induced human lens epithelial cells via miR-124/Slug axis

“…The limitation of this study is that although the TGF-β2induced SRA01/04 cell line is a common in vitro cell model for PCO research (Wang et al, 2019;Zhang et al, 2018), it may not reflect normal lens biology because it does not express many normal lens markers; thus, we cannot determine whether there are potential regulatory differences when compared with the normal lens (Weatherbee et al, 2019). Besides, we only verified the regulatory axis at the cellular level, but not in the animal model.…”

“…Besides, TGF-β2 is the primary subtype of the TGF-β family in aqueous humor (Dong, 2020;Zhang et al, 2017). Therefore, TGF-β2induced human lens epithelial cells (HLECs) can be used to simulate the PCO microenvironment (Wang et al, 2019;Zhang et al, 2017).…”

Knockdown of Tripartite motif-containing 22 (TRIM22)relieved the apoptosis of lens epithelial cells by suppressing the expression of TNF receptor-associated factor 6 (TRAF6)

“…Moreover, the proliferation of lens epithelial cells was associated with the occurrence and development of cataract [ 30 ]. There is also study revealed that the proliferation of lens epithelial cells could induce the occurrence and development of cataract [ 31 ]. We also revealed that the inhibition of TRIM22 rescued the proliferation of lens epithelial cells stimulated by H 2 O 2 .…”

The Emerging Roles of Non-Coding RNAs in Cataract

“…As an example, the elevated KCNQ1OT1 positively regulated SMAD4 expression to promote LEC proliferation and EMT in PCO [31]. LncFEZF1-AS1 promoted the proliferation and migration via upregulating FEZF1 expression in PCO [39]. Upregulated MALAT1 can activate p38, a component of mitogen-activated protein kinases (MAPKs) pathway, resulting in HLECs apoptosis in DC.…”