The relationship between TRAF6 and tumors

Li, Jiaoduan; Liu, Nian; Tang, Ling; Yan, Bei; Chen, Xiang; Zhang, Jianglin; Peng, Cong

doi:10.1186/s12935-020-01517-z

Cited by 34 publications

(35 citation statements)

References 121 publications

(153 reference statements)

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“…Therefore, it is suggested that enhancement of TRAF6 expression in obesity could increase degradation of EZH2, thereby promoting upregulation of miR-429-3p. In addition, TRAF6 also plays a critical role in the activation of nuclear transcription factors associated with adipogenesis and obesity, such as NF-κB and AP-1 [48,49]. In silico analysis of transcription factor binding sites showed that the promoter regions of miR-429-3p contain tentative binding sites for NF-κB and AP-1.…”

Section: Discussionmentioning

confidence: 99%

Palmitic Acid-Induced miR-429-3p Impairs Myoblast Differentiation by Downregulating CFL2

Nguyen

Min

Lee

2021

IJMS

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MicroRNAs are known to play a critical role in skeletal myogenesis and maintenance, and cofilin-2 (CFL2) is necessary for actin cytoskeleton dynamics and myogenic differentiation. Nonetheless, target molecules and the modes of action of miRNAs, especially those responsible for the inhibitory mechanism on the myogenesis by saturated fatty acids (SFA) or obesity, still remain unclear. Here, we reported the role played by miR-429-3p on CFL2 expression, actin filament dynamics, myoblast proliferation, and myogenic differentiation in C2C12 cells. Palmitic acid (PA), the most abundant SFA in diet, inhibited the myogenic differentiation of myoblasts, accompanied by CFL2 reduction and miR-429-3p induction. Interestingly, miR-429-3p suppressed the expression of CFL2 by targeting the 3′UTR of CFL2 mRNA directly. Transfection of miR-429-3p mimic in myoblasts increased F-actin formation and augmented nuclear YAP level, thereby promoting cell cycle progression and myoblast proliferation. Moreover, miR-429-3p mimic drastically suppressed the expressions of myogenic factors, such as MyoD, MyoG, and MyHC, and impaired myogenic differentiation of C2C12 cells. Therefore, this study unveiled the crucial role of miR-429-3p in myogenic differentiation through the suppression of CFL2 and provided implications of SFA-induced miRNA in the regulation of actin dynamics and skeletal myogenesis.

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Section: Discussionmentioning

confidence: 99%

Palmitic Acid-Induced miR-429-3p Impairs Myoblast Differentiation by Downregulating CFL2

Nguyen

Min

Lee

2021

IJMS

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“…In human cancers, genetic changes in the gain and loss of function of different tumor necrosis factor receptor-associated factors (TRAFs) are common [ 19 ]. TRAF6 is the abundantly expressed gene that relates to tumorigenesis and development [ 20 ]. In fact, TRAF6 is the regulatory actor in liver cancer, as to cell apoptosis [ 21 ].…”

Section: Introductionmentioning

confidence: 99%

Silenced lncRNA DDX11-AS1 or up-regulated microRNA-34a-3p inhibits malignant phenotypes of hepatocellular carcinoma cells via suppression of TRAF5

et al. 2021

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Background Studies have discussed long noncoding RNA DDX11-AS1 (DDX11-AS1)-mediated downstream mechanism in hepatocellular carcinoma (HCC). The goal of this study was to investigate the regulatory mechanism of DDX11-AS1-mediated microRNA-34a-3p (miR-34a-3p)/tumor necrosis factor receptor-associated factor 5 (TRAF5) axis on HCC cells. Methods DDX11-AS1, miR-34a-3p and TRAF5 expression levels in HCC were detected. The correlation of DDX11-AS1, miR-34a-3p and TRAF5 in HCC patients was analyzed by Pearson test. HCC cells were transfected with corresponding plasmid/oligonucleotide, and cell proliferation, migration, invasion, apoptosis and tumor formation ability were detected. Bioinformatics software, dual luciferase report experiment and RNA-pull down experiment analysis were applied to verify the targeting relationship between DDX11-AS1, miR-34a-3p and TRAF5. Results Elevated DDX11-AS1 and TRAF5 and reduced miR-34a-3p exhibited in HCC. Silenced DDX11-AS1 or up-regulated miR-34a-3p inhibited the proliferation, migration, invasion, promoted apoptosis of HCC cells and repressed the tumor growth in nude mice. In addition, DDX11-AS1 bound to miR-34a-3p to target TRAF5. Silencing TRAF5 or elevating miR-34a-3p expression mitigated up-regulated DDX11-AS1-mediated promotion of tumor growth. Conclusion Silenced DDX11-AS1 or up-regulated miR-34a-3p inhibits HCC cell growth via elevation of TRAF5, which could be of great benefit to find early diagnostic markers for HCC patients.

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“…Interestingly, the dichotomy between ubiquitination and phosphorylation might underlie the differential functions of P-bodies, where phosphorylation favors mRNA storage and ubiquitination favors decay. These PTMs depend on the E3 ubiquitin ligase TRAF6 [117], which is overexpressed in many cancer types and is associated with poor prognosis [118].…”

Section: Box 1 Rnp Granule Functions Beyond Cancer Cellsmentioning

confidence: 99%

Cancer cell adaptability: turning ribonucleoprotein granules into targets

et al. 2021

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Stress granules (SGs) and processing bodies (P-bodies) are membraneless cytoplasmic condensates of ribonucleoproteins (RNPs). They both regulate RNA fate under physiological and pathological conditions, and are thereby involved in the regulation and maintenance of cellular integrity. During tumorigenesis, cancer cells use these granules to thrive, to adapt to the harsh conditions of the tumor microenvironment (TME), and to protect themselves from anticancer treatments. This ability to provide multiple outcomes not only makes RNP granules promising targets for cancer therapy but also emphasizes the need for more knowledge about the biology of these granules to achieve clinical use. In this review we focus on the role of RNP granules in cancer, and on how their composition and regulation might be used to elaborate therapeutic strategies. RNP granules between stress and translationRegulating the expression of the genomic information is crucial to ensure cell identity and functionality. During transformation into cancer cells and throughout tumor progression, cells dynamically modulate the expression of their genomic information to adapt to environmental cues. Control of mRNA translation ensures the spatiotemporal adjustment of protein synthesis, and is often dysregulated in cancer cells to favor their adaptability [1]. In particular, regulation of translation initiation allows cancer cells to reprogram this activity towards essential mRNAs, such as those encoding oncogenes, to facilitate cell growth, proliferation, and survival [2]. Moreover, cancer cells must adapt to stress conditions in the TME, mainly through activation of the integrated stress response (ISR) [3,4] (Figure 1). This pathway controls translation initiation through eukaryotic initiation factor 2 (eIF2), which, once phosphorylated on its α subunit, prevents the formation of the ternary complex (eIF2:GTP: methionyl-initiator-tRNA) and consequently blocks translation initiation [5]. Four stress-sensor kinases can induce eIF2α phosphorylation, namely the PKR-like endoplasmic reticulum kinase (PERK), general control nonrepressible 2 (GCN2), heme-regulated inhibitor (HRI), and protein kinase R (PKR). The outcome of ISR activation is a global decrease in protein synthesis, while sparing the translation of some specific mRNAs such as that of transcription factor ATF4 [4]. Activation of this pathway, and the resulting selective translation, favor tumor progression following endoplasmic reticulum stress caused for instance by the hypoxic TME [6]. Furthermore, ISR activation by aberrant MYC expression enables cancer cells to adapt to this intrinsic stress by reprogramming translational programs. Consequently, the ISR prevents cancer cells from entering apoptosis and promotes both tumor progression [7,8] and escape from antitumor immunity [9,10].

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The relationship between TRAF6 and tumors

Cited by 34 publications

References 121 publications

Palmitic Acid-Induced miR-429-3p Impairs Myoblast Differentiation by Downregulating CFL2

Palmitic Acid-Induced miR-429-3p Impairs Myoblast Differentiation by Downregulating CFL2

Silenced lncRNA DDX11-AS1 or up-regulated microRNA-34a-3p inhibits malignant phenotypes of hepatocellular carcinoma cells via suppression of TRAF5

Cancer cell adaptability: turning ribonucleoprotein granules into targets

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