α-Arrestin ARRDC3 tumor suppressor function is linked to GPCR-induced TAZ activation and breast cancer metastasis

Arakaki, Aleena; Pan, Wen‐An; Wedegaertner, Helen; Roca-Mercado, Ivette; Chinn, Logan; Gujral, Taranjit S.; Trejo, JoAnn

doi:10.1242/jcs.254888

Cited by 24 publications

(27 citation statements)

References 44 publications

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“…Finally, the internalized receptors are sorted either by degradation or recycling [ 18 ]. Several studies have been done that show the involvement of these GRKs and arrestins in cancer development and progression ( Figure 1 ) [ 18 , 19 , 20 , 21 ].…”

Section: Gpcrs Gpcr Signaling and Cross-talkmentioning

confidence: 99%

An Insight into GPCR and G-Proteins as Cancer Drivers

Chaudhary

Kim

2021

Cells

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G-protein-coupled receptors (GPCRs) are the largest family of cell surface signaling receptors known to play a crucial role in various physiological functions, including tumor growth and metastasis. Various molecules such as hormones, lipids, peptides, and neurotransmitters activate GPCRs that enable the coupling of these receptors to highly specialized transducer proteins, called G-proteins, and initiate multiple signaling pathways. Integration of these intricate networks of signaling cascades leads to numerous biochemical responses involved in diverse pathophysiological activities, including cancer development. While several studies indicate the role of GPCRs in controlling various aspects of cancer progression such as tumor growth, invasion, migration, survival, and metastasis through its aberrant overexpression, mutations, or increased release of agonists, the explicit mechanisms of the involvement of GPCRs in cancer progression is still puzzling. This review provides an insight into the various responses mediated by GPCRs in the development of cancers, the molecular mechanisms involved and the novel pharmacological approaches currently preferred for the treatment of cancer. Thus, these findings extend the knowledge of GPCRs in cancer cells and help in the identification of therapeutics for cancer patients.

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Section: Gpcrs Gpcr Signaling and Cross-talkmentioning

confidence: 99%

An Insight into GPCR and G-Proteins as Cancer Drivers

Chaudhary

Kim

2021

Cells

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“…For example, TXNIP stabilizes the cyclin-dependent kinase inhibitor p27 KIP1 [375]. While a similar TS role for ARRDC4 is lacking, recent work indicates that its paralogs ARRDC1 and ARRDC3 may fulfill a similar function [211,212,376,377].…”

Section: Mondoamentioning

confidence: 99%

Normal and Neoplastic Growth Suppression by The Extended Myc Network

Wang¹,

Prochownik²

2022

Preprint

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Among the first discovered and most prominent cellular oncogenes is MYC, which encodes a bHLH-ZIP transcription factor (Myc) that both activates and suppresses numerous genes involved in proliferation, energy production, metabolism and translation. Myc belongs to a small group of bHLH-ZIP transcriptional regulators (the Myc Network) that includes its obligate heterodimerization partner Max and six “Mxd proteins” (Mxd1-4, Mnt and Mga) each of which heterodimerizes with Max and largely oppose Myc’s functions. More recently, a second group of bHLH-ZIP proteins (the Mlx Network) has emerged. It is comprised of the Myc-like factors ChREBP and MondoA, which, in association with the Max-like member Mlx, regulate smaller and more functionally restricted sets of target genes, some of which are shared with Myc. Opposing ChREBP and MondoA are heterodimers comprised of Mlx and Mxd1, Mxd4 and Mnt, which also structurally and operationally link the two Networks. We discuss here the functions of these “Extended Myc Network” members with particular emphasis on the roles played by Max, Mlx and Mxd proteins in suppressing normal and neoplastic growth. These roles are complex due to the temporally- and tissue-restricted expression of Extended Myc Network proteins in normal cells, their regulation of both common and unique target genes and, in some cases, their functional redundancy.

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“…The first cervical cancer GWAS in the Japanese population failed to identify any SNPs at genome-wide significance, but a second, larger GWAS in the East Asian population (with cohorts from China and Japan), identified and linked their top novel variant rs59661306 on chromosome 5q to the ARRDC3 (Arrestin domain-containing 3) gene, encoding a known tumour suppressor and regulator of insulin sensitivity [119,[149][150][151]. However, these results have not yet been replicated in European populations.…”

Section: Other Gwas Loci For Cervical Cancer or Dysplasiamentioning

confidence: 99%

Genomic Risk Factors for Cervical Cancer

Ramachandran

Dörk

2021

Cancers

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Cervical cancer is the fourth common cancer amongst women worldwide. Infection by high-risk human papilloma virus is necessary in most cases, but not sufficient to develop invasive cervical cancer. Despite a predicted genetic heritability in the range of other gynaecological cancers, only few genomic susceptibility loci have been identified thus far. Various case-control association studies have found corroborative evidence for several independent risk variants at the 6p21.3 locus (HLA), while many reports of associations with variants outside the HLA region remain to be validated in other cohorts. Here, we review cervical cancer susceptibility variants arising from recent genome-wide association studies and meta-analysis in large cohorts and propose 2q14 (PAX8), 17q12 (GSDMB), and 5p15.33 (CLPTM1L) as consistently replicated non-HLA cervical cancer susceptibility loci. We further discuss the available evidence for these loci, knowledge gaps, future perspectives, and the potential impact of these findings on precision medicine strategies to combat cervical cancer.

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α-Arrestin ARRDC3 tumor suppressor function is linked to GPCR-induced TAZ activation and breast cancer metastasis

Cited by 24 publications

References 44 publications

An Insight into GPCR and G-Proteins as Cancer Drivers

An Insight into GPCR and G-Proteins as Cancer Drivers

Normal and Neoplastic Growth Suppression by The Extended Myc Network

Genomic Risk Factors for Cervical Cancer

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