Silencing of Armadillo Repeat-Containing Protein 8 (ARMc8) Inhibits TGF--Induced EMT in Bladder Carcinoma UMUC3 Cells

Liu, Xuan; Men, Qun-Li; Li, Yongwei; Li, Hecheng; Chong, Tie; Li, Zhaolun

doi:10.3727/096504016x14719078133609

Cited by 14 publications

(12 citation statements)

References 26 publications

(8 reference statements)

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“…Knockdown of Armc8 in the hepatocellular carcinoma HepG2 cell line significantly up-regulated the expression levels of E-cadherin, β-catenin and αE-catenin [9]. Silencing of Armc8 inhibited TGF-β-induced epithelial–mesenchymal transduction in bladder carcinoma UMUC3 cells [35]. These findings emphasize that Armc8 is negatively involved in the regulation of the CCC complex.…”

Section: Discussionmentioning

confidence: 99%

Armc8 is an evolutionarily conserved armadillo protein involved in cell–cell adhesion complexes through multiple molecular interactions

et al. 2019

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Armadillo-repeat-containing protein 8 (Armc8) belongs to the family of armadillo-repeat containing proteins, which have been found to be involved in diverse cellular functions including cell–cell contacts and intracellular signaling. By comparative analyses of armadillo repeat protein structures and genomes from various premetazoan and metazoan species, we identified orthologs of human Armc8 and analyzed in detail the evolutionary relationship of Armc8 genes and their encoded proteins. Armc8 is a highly ancestral armadillo protein although not present in yeast. Consequently, Armc8 is not the human ortholog of yeast Gid5/Vid28. Further, we performed a candidate approach to characterize new protein interactors of Armc8. Interactions between Armc8 and specific δ-catenins (plakophilins-1, -2, -3 and p0071) were observed by the yeast two-hybrid approach and confirmed by co-immunoprecipitation and co-localization. We also showed that Armc8 interacts specifically with αE-catenin but neither with αN-catenin nor with αT-catenin. Degradation of αE-catenin has been reported to be important in cancer and to be regulated by Armc8. A similar process may occur with respect to plakophilins in desmosomes. Deregulation of desmosomal proteins has been considered to contribute to tumorigenesis.

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Section: Discussionmentioning

confidence: 99%

Armc8 is an evolutionarily conserved armadillo protein involved in cell–cell adhesion complexes through multiple molecular interactions

et al. 2019

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“…TGF-β1 actions in bladder cancer are also mediated by ARMc8 (Armadillo repeat-containing protein 8). Specifically, ARMc8 mediates TGF-β1-induced migration and invasion, as well as epithelial-mesenchymal transition [203]. Pro-cancerous TGF-β effects are counteracted by protein phosphatase PPM1A, which dephosphorylates SMAD2/3 TGF-β effectors.…”

Section: Bladder Cancermentioning

confidence: 99%

TGF-β and microRNA Interplay in Genitourinary Cancers

Bogusławska¹,

Kryst

Poletajew

et al. 2019

Cells

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Genitourinary cancers (GCs) include a large group of different types of tumors localizing to the kidney, bladder, prostate, testis, and penis. Despite highly divergent molecular patterns, most GCs share commonly disturbed signaling pathways that involve the activity of TGF-β (transforming growth factor beta). TGF-β is a pleiotropic cytokine that regulates key cancer-related molecular and cellular processes, including proliferation, migration, invasion, apoptosis, and chemoresistance. The understanding of the mechanisms of TGF-β actions in cancer is hindered by the “TGF-β paradox” in which early stages of cancerogenic process are suppressed by TGF-β while advanced stages are stimulated by its activity. A growing body of evidence suggests that these paradoxical TGF-β actions could result from the interplay with microRNAs: Short, non-coding RNAs that regulate gene expression by binding to target transcripts and inducing mRNA degradation or inhibition of translation. Here, we discuss the current knowledge of TGF-β signaling in GCs. Importantly, TGF-β signaling and microRNA-mediated regulation of gene expression often act in complicated feedback circuits that involve other crucial regulators of cancer progression (e.g., androgen receptor). Furthermore, recently published in vitro and in vivo studies clearly indicate that the interplay between microRNAs and the TGF-β signaling pathway offers new potential treatment options for GC patients.

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“…ARMC8 downregulation in bladder cancer cells inhibited the TGF β 1-induced migration and invasion and suppressed the EMT progress. Furthermore, ARMC8 silencing inhibited the TGF β 1-induced expression of β -catenin, cyclin D1, and c-myc [95]. Therefore, although via a different signaling pathway, ARMC8 seems to affect some of the same major targets of the WNT signaling.…”

Section: Ctlh Complex Members: Tumor Suppressors or Oncogenes? Drimentioning

confidence: 99%

The CTLH Complex in Cancer Cell Plasticity

Huffman

Palmieri

Coppola

2019

Journal of Oncology

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Cancer cell plasticity is the ability of cancer cells to intermittently morph into different fittest phenotypic states. Due to the intrinsic capacity to change their composition and interactions, protein macromolecular complexes are the ideal instruments for transient transformation. This review focuses on a poorly studied mammalian macromolecular complex called the CTLH (carboxy-terminal to LisH) complex. Currently, this macrostructure includes 11 known members (ARMC8, GID4, GID8, MAEA, MKLN1, RMND5A, RMND5B, RANBP9, RANBP10, WDR26, and YPEL5) and it has been shown to have E3-ligase enzymatic activity. CTLH proteins have been linked to all fundamental biological processes including proliferation, survival, programmed cell death, cell adhesion, and migration. At molecular level, the complex seems to interact and intertwine with key signaling pathways such as the PI3-kinase, WNT, TGFβ, and NFκB, which are key to cancer cell plasticity. As a whole, the CTLH complex is overexpressed in the most prevalent types of cancer and may hold the key to unlock many of the biological secrets that allow cancer cells to thrive in harsh conditions and resist antineoplastic therapy.

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Silencing of Armadillo Repeat-Containing Protein 8 (ARMc8) Inhibits TGF--Induced EMT in Bladder Carcinoma UMUC3 Cells

Cited by 14 publications

References 26 publications

Armc8 is an evolutionarily conserved armadillo protein involved in cell–cell adhesion complexes through multiple molecular interactions

Armc8 is an evolutionarily conserved armadillo protein involved in cell–cell adhesion complexes through multiple molecular interactions

TGF-β and microRNA Interplay in Genitourinary Cancers

The CTLH Complex in Cancer Cell Plasticity

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