Long non-coding RNA highly up-regulated in liver cancer protects tumor necrosis factor-alpha-induced inflammatory injury by down-regulation of microRNA-101 in ATDC5 cells.

Abstract:

BACKGROUND:Osteoarthritis (OA) is a familiar joint degenerative disease. Long non-coding RNAs (lncRNAs) play vital roles in the pathogenesis of OA. Nevertheless, the regulatory impacts of lncRNA highly up-regulated in liver cancer (lncRNA-HULC) on OA remain dimness. The study tried to probe the protective effect of HULC on ATDC5 cells against tumor necrosis factor-alpha (TNF-α)-induced inflammatory injury. METHODS:Relative expression levels of pro-inflammatory cytokines (IL-6, IL-8 and MCP-1) and HULC in OA cartilage tissues and normal cartilage tissues were determined by RT-qPCR. TNF-α induced inflammatory injury model in ATDC5 cells was constructed, and the biological functions of HULC overexpression or suppression in TNF-α-injured ATDC5 cells were assessed. The relevancy between miR-101 and HULC was investigated by utilizing bioinformatics prediction, luciferase reporter assay, RNA pull-down and immunoprecipitation. MiR-101 mimic and inhibitor were transfected into ATDC5 cells, and its regulatory effect on TNF-α-injured ATDC5 cells was examined. Further, NF-κB and MAPK signaling pathways were finally detected by western blot. RESULTS:Enhancement of IL-6, IL-8 and MCP-1 were observated in OA cartilage tissues, but repression of HULC was discovered in OA cartilage tissues. HULC expression was decreased by TNF-α treatment, and overexpressed HULC significantly relieved TNF-α-induced ATDC5 cells injury. Additionally, miR-101 was mutual repressed with HULC, and overexpressed miR-101 reversed the protective effect of HULC in TNF-α-injured ATDC5 cells. Besides, HULC blocked NF-κB and MAPK pathways via repression of miR-101. CONCLUSIONS:The discoveries testified that HULC protected ATDC5 cells against TNF-α-induced inflammatory injury by repression of miR-101.

journal_name

Int Immunopharmacol

authors

Chu P,Wang Q,Wang Z,Gao C

doi

10.1016/j.intimp.2019.04.004

subject

Has Abstract

pub_date

2019-07-01 00:00:00

pages

148-158

eissn

1567-5769

issn

1878-1705

pii

S1567-5769(18)30689-1

journal_volume

72

pub_type

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