RETRACTED: Overexpression of long non-coding RNA TUG1 alleviates TNF-α-induced inflammatory injury in interstitial cells of Cajal (Retracted article. See vol. 27, pg. 5946, 2023)

OBJECTIVE: Irritable bowel syndrome (IBS) is a common functional disorder in the gastrointestinal tract. Inflammatory response has been found to participate in the pathogenesis of IBS. This study aimed to explore the effects of long non-coding RNA taurine upregulated gene 1 (TUG1) on tumor necrosis factor alpha (TNF-alpha)-induced interstitial cells of Cajal (ICC) inflammatory injury, which was relevant to the pathogenesis of IBS. PATIENTS AND METHODS: The expression levels of TUG1 and microRNA-127 (miR-127) were analyzed by qRT-PCR. Viability, apoptosis and the expression of apoptosis-associated factors were analyzed by CCK-8 assay, flow cytometry and Western blot, respectively. The mRNA and protein levels of pro-inflammatory cytokines were detected by qRT-PCR and Western blot, respectively. Finally, activations of nuclear factor kappa-B (NF-kappa B) and Notch pathways were evaluated by Western blot. RESULTS: TNF-alpha treatment inhibited ICC viability, induced ICC apoptosis and promoted an inflammatory response in ICC. TUG1 was down regulated in TNF-alpha-treated ICC. TUG1 overexpression protected ICC from TNF-alpha-induced apoptosis and pro-inflammatory cytokines expression. TUG1 suppression showed opposite effects. MiR-127 was negatively regulated by TUG1 and implicated in the action of TUG1 in ICC. MiR-127 up-regulation largely reversed the effects of TUG1 on TNF-alpha-treated ICC. Mechanistically, TUG1 inhibited TNF-alpha-induced activation of NF-kappa B and Notch pathways in ICC by down-regulating miR-127. CONCLUSIONS: TUG1 attenuated TNF-alpha-caused apoptosis and inflammatory response in ICC by down-regulating miR-127 and then inactivating NF-kappa B and Notch pathways.