MicroRNA-708 prevents ethanol-induced hepatic lipid accumulation and inflammatory reaction via direct targeting ZEB1

Hu, Shuang; Liu, Yumin; Chenchen,; Li, Liang-yun; Zhang, Bo-yu; Yang, Jun; Li, Haodong; Meng, Xiao‐Ming; Junli,; Xu, Tao; Zhou, Huan

doi:10.1016/j.lfs.2020.118147

Cited by 14 publications

(13 citation statements)

References 23 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…It has been reported that ZEB1 is implicated in inflammatory response. For example, miR-708 inhibited liver inflammation and lipid accumulation via targeting ZEB1 [ 13 ]. In addition, ZEB1 promoted inflammation via suppressing the DNA repair glycosylase MPG in epithelial cells [ 14 ].…”

Section: Introductionmentioning

confidence: 99%

MicroRNA-128-3p suppresses interleukin-1β-stimulated cartilage degradation and chondrocyte apoptosis via targeting zinc finger E-box binding homeobox 1 in osteoarthritis

et al. 2022

View full text Add to dashboard Cite

Accumulating studies have suggested that microRNAs (miRNAs) play vital roles in the pathogenesis of osteoarthritis (OA). Nevertheless, the specific function of miR-128-3p in OA remains unknown. In this study, we demonstrated that miR-128-3p was decreased and ZEB1 was increased in OA. Additionally, miR-128-3p expression was negatively correlated with ZEB1. miR-128-3p overexpression or ZEB1 silencing attenuated extracellular matrix degradation and cell apoptosis, and increased the proliferation of IL-1β-activated CHON-001 cells. Furthermore, ZEB1 was directly targeted by miR-128-3p. In addition, ZEB1 upregulation restored the effects of miR-128-3p overexpression on OA progression. Overall, our findings suggested that miR-128-3p might regulate the development of OA via targeting ZEB1.

show abstract

Section: Introductionmentioning

confidence: 99%

MicroRNA-128-3p suppresses interleukin-1β-stimulated cartilage degradation and chondrocyte apoptosis via targeting zinc finger E-box binding homeobox 1 in osteoarthritis

et al. 2022

View full text Add to dashboard Cite

show abstract

“…Additionally, forced overexpression of miR-708 in human airway smooth muscle cells decreased expression of asthma-related genes [20]. miR-708 also decreased alcohol-induced liver inflammation by targeting zinc finger E-box-binding homeobox 1 (ZEB-1) upregulation of TNFα and IL-6 [21]. Lastly, injections of miR-708 mimic into a rodent RA model ameliorated the RA index by inhibiting WNT signaling [22].…”

Section: Introductionmentioning

confidence: 98%

miR-708 Negatively Regulates TNFα/IL-1β Signaling by Suppressing NF-κB and Arachidonic Acid Pathways

Monteleone

Lutz

2021

Mediators of Inflammation

View full text Add to dashboard Cite

Two pathways commonly dysregulated in autoimmune diseases and cancer are tumor necrosis factor alpha (TNFα) and interleukin 1 beta (IL-1β) signaling. Researchers have also shown that both signaling cascades positively regulate arachidonic acid (AA) signaling. More specifically, TNFα/IL-1β promotes expression of the prostaglandin E2- (PGE2-) producing enzymes, cyclooxygenase-2 (COX-2) and microsomal prostaglandin E synthase-1 (mPGES-1). Exacerbated TNFα, IL-1β, and AA signaling have been associated with many diseases. While some TNFα therapies have significantly improved patients’ lives, there is still an urgent need to develop novel therapeutics that more comprehensively treat inflammatory-related diseases. Recently, researchers have begun to use RNA interference (RNAi) to treat various diseases in the clinic. One type of RNAi is microRNA (miRNA), a class of small noncoding RNA found within cells. One miRNA in particular, miR-708, has been shown to target COX-2 and mPGES-1. Previous studies have also suggested that miR-708 may be a negative regulator of TNFα/IL-1β signaling. Therefore, we studied the relationship between miR-708, TNFα/IL-1β, and AA signaling in diseased lung cells. We found that miR-708 negatively regulates TNFα/IL-1β signaling in nondiseased lung cells, which is lost in diseased lung cells. Transient transfection of miR-708 suppressed TNFα/IL-1β-induced changes in COX-2, mPGES-1, and PGE2 levels. Moreover, miR-708 also suppressed TNFα/IL-1β-induced IL-6 independent of AA signaling. Mechanistically, we determined that miR-708 suppressed IL-6 signaling by reducing expression of the nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) activator inhibitor of nuclear factor kappa-B kinase subunit beta (IKKβ). Collectively, our data suggest miR-708 regulates TNFα/IL-1β signaling by inhibiting multiple points of the signaling cascade.

show abstract

Section: Introductionmentioning

confidence: 99%

“…Increasing evidence has revealed that lipid metabolism plays an important part in the high capability of HCC cells to uptake glucose (17)(18)(19). Almost 60% of the glucose taken up by HCC cells is used for the synthesis of fatty acids (17)(18)(19). Sterol regulatory element binding protein (SREBP)-1 is the most important transcription factor in lipid metabolism (20)(21)(22).…”

Section: Introductionmentioning

confidence: 99%

“…Sterol regulatory element binding protein (SREBP)-1 is the most important transcription factor in lipid metabolism (20)(21)(22). In HCC cells, SREBP-1 mediates the transcription of genes related to the syntheses of fatty acids and triglycerides (17)(18)(19). Inhibition of activation of SREBP-1 via small-molecule inhibitors or small interfering (si)RNAs of SREBP-1 not only reduces the syntheses of fatty acids and triglycerides, it also inhibits glucose uptake (23,24).…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Inhibition of SREBP-1 Activation by a Novel Small-Molecule Inhibitor Enhances the Sensitivity of Hepatocellular Carcinoma Tissue to Radiofrequency Ablation

2021

View full text Add to dashboard Cite

Radiofrequency ablation (RFA) is an important strategy for treatment of advanced hepatocellular carcinoma (HCC). However, the prognostic indicators of RFA therapy are not known, and there are few strategies for RFA sensitization. The transcription factor sterol regulatory element binding protein 1 (SREBP)-1 regulates fatty-acid synthesis but also promotes the proliferation or metastasis of HCC cells. Here, the clinical importance of SREBP-1 and potential application of knockdown of SREBP-1 expression in RFA of advanced HCC was elucidated. In patients with advanced HCC receiving RFA, a high level of endogenous SREBP-1 expression correlated to poor survival. Inhibition of SREBP-1 activation using a novel small-molecule inhibitor, SI-1, not only inhibited the aerobic glycolysis of HCC cells, it also enhanced the antitumor effects of RFA on xenograft tumors. Overall, our results: (i) revealed the correlation between SREBP-1 and HCC severity; (ii) indicated that inhibition of SREBP-1 activation could be a promising approach for treatment of advanced HCC.

show abstract

MicroRNA-708 prevents ethanol-induced hepatic lipid accumulation and inflammatory reaction via direct targeting ZEB1

Cited by 14 publications

References 23 publications

MicroRNA-128-3p suppresses interleukin-1β-stimulated cartilage degradation and chondrocyte apoptosis via targeting zinc finger E-box binding homeobox 1 in osteoarthritis

MicroRNA-128-3p suppresses interleukin-1β-stimulated cartilage degradation and chondrocyte apoptosis via targeting zinc finger E-box binding homeobox 1 in osteoarthritis

miR-708 Negatively Regulates TNFα/IL-1β Signaling by Suppressing NF-κB and Arachidonic Acid Pathways

Inhibition of SREBP-1 Activation by a Novel Small-Molecule Inhibitor Enhances the Sensitivity of Hepatocellular Carcinoma Tissue to Radiofrequency Ablation

Contact Info

Product

Resources

About