RETRACTION: LncRNA TUG1 Promotes the Intervertebral Disc Degeneration and Apoptosis of Nucleus Pulposus Cell by Modulating NF-κB Signal Pathway

Chunqiang Bi^#, Zilong Ma^#, Xue Song^*, Shuqin Zhang^*

THE AUTHORS HAVE EXPRESSED THE WILL TO WITHDRAW THE PAPER. THE PUBLISHER "CARBONE EDITORE SRL" HAS ACCEPTED THEIR REQUEST. 

The link of the retracted article:

https://www.actamedicamediterranea.com/archive/2022/medica-2/retraction-effect-of-topical-traumatic-drug-on-expression-of-il-6-inmuscle-cells-of-new-zealand-rabbits-after-exercise-induced-chronic-skeletal-muscle-injury/document

Introduction: To investigate the role of long non-coding RNA taurine upregulating gene 1 (TUG1) in the intervertebral disc degeneration and apoptosis of nucleus pulposus cells and the relevant molecular mechanism.

Materials: NP samples for this study were collected from 15 LDH patients (Case group) who accepted the surgery in South District of Guang'anmen Hospital between January 2019 to January 2022.

Methods: Human degenerative nucleus pulposus (NP) samples were collected from 15 lumbar disc herniation (LDH) patients (treatment group) who received the surgery of lumbar vertebra, while the normal NP samples from 15 patients with the fracture of lumbar vertebra. Those samples were then subjected to the real-time fluorescent quantitative polymerase chain reaction and Western blot to determine the expression profiles of TUG1, miR-26a and NF-κB, and the RNA-binding protein immunoprecipitation to validate the relationship between TUG1 and miR-26a.

Results: TUG1 protein expression was up-regulated evidently in the human degenerative NPCs and normal NPCs, while miR-26a expression was down-regulated remarkably. TUG1 overexpression could inhibit the proliferation, while promote the apoptosis of human degenerative NPCs and degradation of extracellular matrix (ECM). TUG1, as an endogenous sponge, could down-regulate the expression of miR-26a in NPCs by binding to miR-26a directly. MiR-26a overexpression could abolish the effect of TUG1 overexpression on the apoptosis of NPCs and ECM degradation; TUG1 overexpression could up-regulate the expression of p65 in the nucleus and simultaneously eliminated partially the inhibitory effect of pre-treatment of QNZ on the NF-κB.

Conclusion: TUG1 could promote the apoptosis of degenerative NPCs and ECM degradation in the intervertebral disc by modulating the miR-26a/NF-κB axis.