TRAF6 Promotes Gastric Cancer Cell Self-Renewal, Proliferation, and Migration

Yang, Mengting; Jin, Meng; Li, Kailong; Liu, Haifeng; Yang, Xiaonan; Zhang, Xiaobei; Zhang, Bin; Gong, Aihua; Bie, Qingli

doi:10.1155/2020/3296192

Cited by 17 publications

(15 citation statements)

References 45 publications

(50 reference statements)

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“…Interestingly, the binding relation between TRAF6 mRNA and METTL3 has been verified in microglia [32] . TRAF6 is a notable oncogene in esophageal squamous cell carcinoma, pancreatic cancer, prostate cancer, nasopharyngeal carcinoma, and gastric cancer [33] , [34] , [35] , [36] , [37] . Moreover, the expression of Vimentin was downregulated and that of E-cadherin was elevated after TRAF6 knockdown in cancer stem cells of squamous cell carcinoma of head and neck [38] , indicating the possible role of TRAF6 in regulating the EMT event.…”

Section: Discussionmentioning

confidence: 99%

m6A-dependent upregulation of TRAF6 by METTL3 is associated with metastatic osteosarcoma

Wang

Huang

et al. 2022

Journal of Bone Oncology

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Section: Discussionmentioning

confidence: 99%

m6A-dependent upregulation of TRAF6 by METTL3 is associated with metastatic osteosarcoma

Wang

Huang

et al. 2022

Journal of Bone Oncology

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“…Smad2 and Smad3 are phosphorylated by TGF-b1 signals, then form hetero trimeric complexes about Smad4, translocating into the nucleus, activating the expression level of EMT-TFs, and cooperating with these transcription factors to regulate EMTrelated genes (79). In addition, non-Smad pathways are also involved in the TGF-b1-induced EMT process, such as phosphatidylinositol 3-kinase (PI3K)/AKT/mammalian TOR complex 1 (mTORC1), tumor necrosis factor receptorassociated factor 6 (TRAF6)/TGF b-Activated Kinase 1 (TAK1), and Wnt/b-catenin signaling (80)(81)(82).…”

Section: The Emt Processmentioning

confidence: 99%

Resveratrol and Its Analogs: Potent Agents to Reverse Epithelial-to-Mesenchymal Transition in Tumors

et al. 2021

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Epithelial-to-mesenchymal transition (EMT), a complicated program through which polarized epithelial cells acquire motile mesothelial traits, is regulated by tumor microenvironment. EMT is involved in tumor progression, invasion and metastasis via reconstructing the cytoskeleton and degrading the tumor basement membrane. Accumulating evidence shows that resveratrol, as a non-flavonoid polyphenol, can reverse EMT and inhibit invasion and migration of human tumors via diverse mechanisms and signaling pathways. In the present review, we will summarize the detailed mechanisms and pathways by which resveratrol and its analogs (e.g. Triacetyl resveratrol, 3,5,4’-Trimethoxystilbene) might regulate the EMT process in cancer cells to better understand their potential as novel anti-tumor agents. Resveratrol can also reverse chemoresistance via EMT inhibition and improvement of the antiproliferative effects of conventional treatments. Therefore, resveratrol and its analogs have the potential to become novel adjunctive agents to inhibit cancer metastasis, which might be partly related to their blocking of the EMT process.

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“…Previous studies have reported that EMT may be related to the stemness of CSCs (25)(26)(27). Therefore, whether RORβ played a role in modulating the metastatic ability of GC cells was investigated.…”

Section: Rorβ Confers Resistance To Emt In Gc Cellsmentioning

confidence: 99%

RORβ suppresses the stemness of gastric cancer cells by downregulating the activity of the Wnt signaling pathway

Wen

Guo

et al. 2021

Oncol Rep

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Gastric cancer (GC) is the third leading cause of cancer-related mortality and the fifth most common type of cancer worldwide. GC stem cells (GCSCs) have been reported to be responsible for the malignant behavior of GC. However, the key molecular mechanism controlling GCSC function remains unclear. The present study aimed to investigate the function of retinoic acid-related orphan receptor β (RORβ) in GC. The expression levels of RORβ in GC cells and clinical GC tissues were analyzed using western blotting, reverse transcription-quantitative PCR (RT-qPCR) and immunohistochemistry. The association between RORβ expression levels and GCSC markers was analyzed using Gene Set Enrichment Analysis, and GeneChip was performed to identify differentially expressed genes between control and RORβ-overexpressing GC cells. CCK-8 and flow cytometric assays were used to evaluate the effect of RORβ on cell viability and apoptosis, respectively. The effect of RORβ on the self-renewal capacity of GCSCs was measured using a sphere formation assay, the expression levels of induced pluripotent stem (iPS) factors and epithelial-mesenchymal transition (EMT)-related factors were measured by RT-qPCR and western blotting, and the tumorigenic capacity was measured by an in vivo mouse model. Finally, the impact of RORβ on the Wnt signaling pathway was determined using western blotting and a TOP/FOP flash assay. The results revealed that the expression levels of RORβ were downregulated in GC tissues compared with para-carcinoma tissues, and were inversely associated with the expression levels of GCSC markers. The overexpression of RORβ upregulated the expression levels of the pro-apoptotic gene, Bcl-2 like protein 11, which subsequently inhibited the viability and promoted the apoptosis of GC cells. In addition, RORβ decreased the sphere forming ability, and downregulated the expression levels of iPS cell-and EMT-related factors. In vivo, RORβ suppressed the tumorigenic capacity and stemness of GC cells. Mechanistically, RORβ was revealed to decrease the activity of the Wnt/β-catenin signaling pathway in GCSCs. In conclusion, the findings of the present study identified RORβ as a novel suppressor of GCSCs and highlighted the prospect of RORβ as a novel candidate target for stem cell-based GC therapy.

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TRAF6 Promotes Gastric Cancer Cell Self-Renewal, Proliferation, and Migration

Cited by 17 publications

References 45 publications

m6A-dependent upregulation of TRAF6 by METTL3 is associated with metastatic osteosarcoma

m6A-dependent upregulation of TRAF6 by METTL3 is associated with metastatic osteosarcoma

Resveratrol and Its Analogs: Potent Agents to Reverse Epithelial-to-Mesenchymal Transition in Tumors

RORβ suppresses the stemness of gastric cancer cells by downregulating the activity of the Wnt signaling pathway

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