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lncRNA TUG1 regulates ulcerative colitis through miR-142-5p/SOCS1 axis
Jing Han1, Yawei Li2, Baolian Zhang3
1Department of Gastroenterology, The East Branch of the Second Hospital of Hebei Medical University, No.80 Huanghe Road, Shijiazhuang, 050000, Hebei, China; Department of Physical Examination Center, The North Branch of the Second Hospital of Hebei Medical University, No. 309 Zhonghua Street, Shijiazhuang, 050000, Hebei, China.
Abstract:
Ulcerative colitis (UC) is a long-lasting inflammation disease which finally results in ulcer of the colon and rectum. The long non-coding RNA (lncRNA) TUG1 has been described to target miR-142 and regulate its expression. In current study, we evaluated the effects of long non-coding RNA TUG1 on cell injury and inflammatory cytokine production using a TNFα-treated HT-29 cells model. We monitored the level of TUG1 in colonic mucosa tissue of UC patients and in TNF-α-treated HT-29 cells. We investigated the effects of TUG1 on miR-142-5p and SOCS1expression, cell viability, lactate dehydrogenase (LDH) release, production of nitrite and PGE2 after TNF-α treatment in HT-29 cells. We also investigated the effects of TUG1 on TNF-α-induced IL-6, IL-8 and IL-1β expression in HT-29 cells. We detected down-regulated TUG1 level in colonic mucosa tissue of UC patients and in TNF-α-treated HT-29 cells. Overexpression of TUG1 enhanced cell viability, decreased LDH release, decreased nitrite and PGE2 production after TNF-α treatment in HT-29 cells. TUG1 prevented IL-1β, IL-6 and IL-8 production in TNF-α-treated cells. TUG1 targeted miR-142-5p and inhibited its expression while enhanced SOCS1 expression. Overexpression of miR-142-5p abolished TUG1-mediated inhibition of TNF-induced inflammatory cytokines production. TUG1 negatively regulated inflammation in ulcerative colitis through miR-142-5p/SOCS1 axis.
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