Current eye research · 2021
Circ-MKLN1/miR-377-3p/CTGF Axis Regulates the TGF-β2-induced Posterior Capsular Opacification in SRA01/04 Cells.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод пока не подготовлен
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Liu Jiajia, Dong Yiran, Ji Qingshan, Wen Yuechun, Ke Genjie, Shi Lei, Guan Wei, Xu Weiping
Аннотация
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.
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.