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Circ-MKLN1/miR-377-3p/CTGF Axis Regulates the TGF-β2-induced Posterior Capsular Opacification in SRA01/04 Cells

, , , , , , & ORCID Icon show all
Pages 372-381 | Received 27 May 2021, Accepted 25 Sep 2021, Published online: 27 Dec 2021
 

ABSTRACT

Objective

Posterior capsular opacification (PCO) is a common postoperative ocular complication after cataract surgery. Little research focused on the regulation of circular RNAs (circRNAs) in PCO. This study was designed to investigate the function of circRNA-muskelin (circ-MKLN1) in PCO.

Methods

SRA01/04 cells were treated with transforming growth factor (TGF)-β2. Cell viability was analyzed by Cell Counting Kit-8 (CCK-8) assay. Transwell assay was used for cell migration and invasion detection. Cell migration was also measured by wound healing assay. Epithelial-mesenchymal transition (EMT)-related proteins and connective tissue growth factor (CTGF) were quantified using western blot.

Results

Cell viability, migration, invasion and EMT process in SRA01/04 cells were facilitated by TGF-β2. Circ-MKLN1 expression was enhanced in 17 PCO lens samples relative to 19 normal lens samples and TGF-β2-treated SRA01/04 cells contrasted to control cells. Downregulation of circ-MKLN1 inhibited the effects of TGF-β2 on SRA01/04 cells. Circ-MKLN1 targeted miR-377-3p and the regulation of si-circ-MKLN1 for the TGF-β2-induced influences was related to the upregulation of miR-377-3p. CTGF was the target gene for miR-377-3p. CTGF knockdown also abolished the TGF-β2-mediated cell growth, migration and invasion of SRA01/04 cells. The function of miR-377-3p was achieved by reducing the CTGF level. TGF-β2-induced CTGF expression promotion was alleviated by si-circ-MKLN1 through upregulating the expression of miR-377-3p.

Conclusion

These results showed that circ-MKLN1 contributed to the progression of PCO in vitro by increasing the CTGF expression via sponging miR-377-3p. Circ-MKLN1 might be important for improving the molecular target therapy in PCO.

Disclosure statement

No potential conflict of interest was reported by the author(s).

Additional information

Funding

This work was supported by the National Natural Science Foundation of China [No. 52072360, No.51672004], The Key Research and Development Program of Anhui Province [China, No. 1804h08020252] and the Natural Science Foundation of Anhui Province [China, No. 1608085MH176, 1908085QB65]; the National Natural Science Foundation of China [No. 52072360, No.51672004];the Natural Science Foundation of Anhui Province [China, No. 1608085MH176, 1908085QB65];the Key Research and Development Program of Anhui Province [China, No. 1804h08020252].

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