Abstract:
BACKGROUND:Abnormal proliferation, metastasis and epithelial-mesenchymal transformation (EMT) of lens epithelial cells (LECs) are direct factors of posterior capsular opacification (PCO). Nuclear enriched abundant transcript 1 (NEAT1) has been shown to promote cell proliferation, metastasis and EMT, but whether it affects the progression of PCO is unclear. METHODS:The expression of NEAT1, microRNA-486-5p (miR-486-5p) and Drosophila mothers against decapentaplegic 4 (SMAD4) was determined using quantitative real-time polymerase chain reaction (qRT-PCR). The proliferation of cells was measured via 3-(4, 5-dimethyl-2 thiazolyl)-2, 5-diphenyl-2-H-tetrazolium bromide (MTT) assay. Transwell assay was employed to detect the migration and invasion of cells. The levels of EMT marker proteins, SMAD4 protein and transforming growth factor-β (TGF-β)/SMAD signaling pathway-related proteins were assessed by western blot (WB) analysis. Further, the relationship between miR-486-5p and NEAT1 or SMAD4 was confirmed by dual-luciferase reporter assay, RNA immunoprecipitation (RIP) assay and biotin-labeled RNA pull-down assay. RESULTS:NEAT1 is upregulated and miR-486-5p is downregulated in the posterior capsular tissues of PCO patients and TGF-β2-induced LECs. Interference of NEAT1 reverses the promoting effect of TGF-β2 on the proliferation, migration, invasion and EMT of LECs. MiR-486-5p can be sponged by NEAT1, and its inhibitor reverses the suppression effect of NEAT1 silencing on the progression of TGF-β2-induced LECs. SMAD4 functions as a target of miR-486-5p, and its overexpression recovers the inhibition effect of miR-486-5p overexpression on the progression of TGF-β2-induced LECs. The activity of the TGF-β/SMAD signaling pathway is regulated by the NEAT1/miR-486-5p/SMAD4 axis. CONCLUSION:Our study shows that NEAT1 has a positive effect on the progression of PCO and is expected to become a new target for PCO treatment.
journal_name
Cancer Cell Intjournal_title
Cancer cell internationalauthors
Wang H,Zheng Gdoi
10.1186/s12935-020-01619-8subject
Has Abstractpub_date
2020-10-31 00:00:00pages
529issue
1issn
1475-2867pii
10.1186/s12935-020-01619-8journal_volume
20pub_type
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journal_title:Cancer cell international
pub_type: 杂志文章
doi:10.1186/s12935-020-01289-6
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journal_title:Cancer cell international
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pub_type: 杂志文章
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journal_title:Cancer cell international
pub_type: 杂志文章
doi:10.1186/s12935-020-01700-2
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pub_type: 杂志文章,评审
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pub_type: 杂志文章
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journal_title:Cancer cell international
pub_type: 杂志文章
doi:10.1186/s12935-020-01578-0
更新日期:2020-11-13 00:00:00
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pub_type: 杂志文章
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journal_title:Cancer cell international
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pub_type: 杂志文章
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abstract::[This corrects the article DOI: 10.1186/s12935-017-0407-9.]. ...
journal_title:Cancer cell international
pub_type: 已发布勘误
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更新日期:2020-07-17 00:00:00
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journal_title:Cancer cell international
pub_type: 杂志文章
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更新日期:2014-08-12 00:00:00
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journal_title:Cancer cell international
pub_type: 杂志文章,评审
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abstract:Background:Gastric cancer (GC) is a common cause of cancer-related mortality worldwide, and microRNAs (miRNAs) have been shown to play an important role in GC development. This study aims to explore the effect of microRNA-93-5p (miR-93-5p) on the epithelial-mesenchymal transition (EMT) in GC, via AHNAK and the Wnt sign...
journal_title:Cancer cell international
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journal_title:Cancer cell international
pub_type: 杂志文章
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journal_title:Cancer cell international
pub_type: 杂志文章
doi:10.1186/s12935-016-0352-z
更新日期:2016-09-29 00:00:00
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journal_title:Cancer cell international
pub_type: 杂志文章
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journal_title:Cancer cell international
pub_type: 杂志文章
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