TMEM88 mediates inflammatory cytokines secretion by regulating JNK/P38 and canonical Wnt/β-catenin signaling pathway in LX-2 cells

Xu, Tao; Pan, Linxin; Ge, Yunxuan; Meng, Xiao‐Ming; Huang, Cheng; Li, Jun

doi:10.1007/s10787-017-0419-z

Cited by 18 publications

(13 citation statements)

References 28 publications

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“…Moreover, TMEM88 inhibits Wnt/β‐catenin signaling by enhancing the localization of the β‐catenin‐containing Wnt signalosome to multivesicular bodies, a change that impedes β‐catenin nuclear translocation [24] . Previous studies have shown that TMEM88 exerts its function in various cellular processes via regulation of Wnt/β‐catenin signaling [5‐7,9] . Interestingly, a recent study has revealed that TMEM88 plays the tumor‐suppressive role in thyroid cancer via inhibition of Wnt/β‐catenin signaling [23] .…”

Section: Discussionmentioning

confidence: 99%

“…Although the studies of TMEM88 are limited, the involvement of TMEM88 in multiple pathological processes has been increasingly highlighted. The decreased expression of TMEM88 contributes to progression of hepatic fibrosis, with an effect on the activation of hepatic stellate cells [6,7] . Elevation of TMEM88 leads to an increase in the secretion of inflammatory factors in alcoholic liver disease [8] .…”

Section: Introductionmentioning

confidence: 99%

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TMEM88 exhibits an antiproliferative and anti‐invasive effect in bladder cancer by downregulating Wnt/β‐catenin signaling

Zhao

Chong

et al. 2021

J Biochem & Molecular Tox

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Transmembrane protein 88 (TMEM88) acts as a novel tumor‐associated protein. The dysregulation of TMEM88 has been observed in several tumor types. However, the relevance of TMEM88 in tumorigenesis is still contradictory. This study assessed the relevance of TMEM88 in bladder cancer. TMEM88 levels were found to be significantly lower in bladder cancer tissue. Upregulation of TMEM88 resulted in a dramatic decrease in the cellular proliferative and invasive abilities of bladder cancer. Upregulation of TMEM88 decreased the level of active β‐catenin and prohibited the activation of the Wnt/β‐catenin pathway, an effect that was associated with downregulation of glycogen synthase kinase‐3β (GSK‐3β) phosphorylation. Suppression of GSK‐3β or overexpression of β‐catenin reversed the TMEM88‐induced tumor‐inhibiting effects in bladder cancer. Overexpression of TMEM88 prohibited the tumor formation and growth of bladder cancer cells in nude mice. In conclusion, this study demonstrates that TMEM88 exerts an antitumor function in bladder cancer through downregulation of Wnt/β‐catenin signaling.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

TMEM88 exhibits an antiproliferative and anti‐invasive effect in bladder cancer by downregulating Wnt/β‐catenin signaling

Zhao

Chong

et al. 2021

J Biochem & Molecular Tox

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“…Human pro-monocytic cells U937 cell line was used as a source of inflammatory response cell [46,47]. U937 cell line was resuspended in a Dulbecco’s modified Eagle’s medium (DMEM) 1 g/L D-glucose (Gibco, Life Technologies, Milan, Italy) supplemented with 10% v/v heat-inactivated fetal bovine serum (FBS) (Invitrogen, Carlsbad, CA, USA), 1% penicillin/streptomycin (Carlo Erba, Milan, Italy) antibiotic/antimycotic solution, and 60 mg/mL of gentamicin (Gibco, Monza, Italy).…”

Section: Methodsmentioning

confidence: 99%

Piacentinu Ennese PDO Cheese as Reservoir of Promising Probiotic Bacteria

et al. 2019

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Piacentinu Ennese is a protected designation of origin (PDO) cheese produced in the surrounding area of Enna (Sicily, Italy), using raw ewe’s milk without the addition of any starter cultures. In the present study, the Lactobacillus population of Piacentinu Ennese PDO cheese was in vitro screened in order to select promising probiotic strains to be further used in humans. One hundred and sixty-nine lactic acid bacteria (LAB) were isolated from 90 days ripened cheeses and identified by Rep-PCR genomic fingerprinting, using the (GTG)5-primer, and by MALDI-TOF MS. One hundred and thirteen (113) isolates belonging to QPS-list species were characterized for both safety and functional properties. All tested isolates were considered safe because none showed either gelatinase, DNase, mucinase, or hemolytic activity. Tolerance to lysozyme, bile salts, and acidic conditions, along with ability to survive under simulated gastrointestinal digestion, were observed. In addition, based on antimicrobial activity against pathogens, cell surface characteristics, Caco-2 adhesion abilities, and anti-inflammatory potential, it was possible to confirm the strain-dependent functional aptitude, suggesting that Piacentinu Ennese PDO cheese may be considered a precious source of probiotic candidates.

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“…[7][8][9][10] Notably, activation of HSCs is connected with several inflammatory cytokines, such as IL-6 and IL-1β. 11 It is particularly important to find an effective way to inhibit the expression of macrophages. Lipopolysaccharide (LPS) is the main component of the cell wall of gram-negative bacteria and the level of it is elevated in patients with alcoholic fatty liver or cirrhosis.…”

Section: Introductionmentioning

confidence: 99%

CD73 Attenuates Alcohol-Induced Liver Injury and Inflammation via Blocking TLR4/MyD88/NF-κB Signaling Pathway

Liu¹,

Wu²,

Qian³

et al. 2022

JIR

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Background: Alcoholic liver disease (ALD) is liver damage caused by long-term drinking. Inflammation plays a central role in the progression of ALD. CD73 is a ubiquitously expressed glycosylphosphatidylinositol-anchored glycoprotein that is a key enzyme that converts ATP into adenosine. Evidence has shown that CD73 plays an important role in many diseases, but the role and mechanism of CD73 in alcohol-induced liver injury and inflammation is still unclear. Methods: The alcohol-induced liver injury and inflammation mouse model was established. The rAAV9-CD73 was used to overexpress CD73. Isolation of primary macrophages (MΦ) from the liver was conducted. The effects of CD73 on alcohol-induced liver injury and inflammation were evaluated by quantitative real-time PCR, Western blotting, ELISA, and immunohistochemical assay. Flow cytometry was used to detect the cell cycle and apoptosis. Results: Our results showed that overexpression of CD73 can reduce alcohol-induced liver damage, lipid accumulation, and the secretion of inflammatory cytokines. pEX3-CD73 can promote RAW264.7 cells proliferation and inhibit apoptosis via suppressing the activation of TLR4/MyD88/NF-κB signaling pathway. Inhibition of TLR4 further enhanced the antiinflammatory effect of overexpression of CD73. Conclusion: Overexpression of CD73 can reduce alcohol-induced liver injury and inflammation. CD73 may serve as a potential therapeutic target for ALD.

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TMEM88 mediates inflammatory cytokines secretion by regulating JNK/P38 and canonical Wnt/β-catenin signaling pathway in LX-2 cells

Cited by 18 publications

References 28 publications

TMEM88 exhibits an antiproliferative and anti‐invasive effect in bladder cancer by downregulating Wnt/β‐catenin signaling

TMEM88 exhibits an antiproliferative and anti‐invasive effect in bladder cancer by downregulating Wnt/β‐catenin signaling

Piacentinu Ennese PDO Cheese as Reservoir of Promising Probiotic Bacteria

CD73 Attenuates Alcohol-Induced Liver Injury and Inflammation via Blocking TLR4/MyD88/NF-κB Signaling Pathway

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