Cancer driver G-protein coupled receptor (GPCR) induced β-catenin nuclear localization: the transcriptional junction

Nag, Jeetendra Kumar; Rudina, Tatyana; Maoz, Myriam; Grisaru‐Granovsky, Sorina; Uziely, Beatrice; Bar-Shavit, Rachel

doi:10.1007/s10555-017-9711-z

Cited by 13 publications

(9 citation statements)

References 105 publications

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“…In GPCR‐dependent signaling, β‐arrestins facilitate receptor internalization and stimulate downstream targets such as AKT, GSK3β, and Wnt/β‐catenin signaling 12 . β‐Catenin is a critical regulator and transducer of GPCRs, which play roles in various physiological and pathological processes in cancer growth 40 . Moreover, β‐catenin also plays a critical role in promoting EMT by regulating the expression of EMT‐related transcription factors 41,42 .…”

Section: Discussionmentioning

confidence: 99%

Retracted: Overexpression of dopamine receptor D2 promotes colorectal cancer progression by activating the β‐catenin/ZEB1 axis

Lee¹,

Shim²,

Kong

et al. 2021

Cancer Science

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Colorectal cancer (CRC) is a recurring cancer that is often resistant to conventional therapies and therefore requires the development of molecular‐based therapeutic approaches. Dopamine receptor D2 (DRD2) is associated with the growth of many types of tumors, but its oncogenic role in CRC is unclear. Here, we observed that elevated DRD2 expression was associated with a poor survival rate among patients with CRC. Depletion of DRD2 suppressed CRC cell growth and motility by downregulating β‐catenin/ZEB signaling in vitro and in vivo, whereas overexpression of DRD2 promoted CRC cell progression. Inhibition of DRD2 by the antagonist pimozide inhibited tumor growth and lymph node metastasis in vivo and enhanced the cytotoxic effects of conventional agents in vitro. Taken together, our findings indicate that targeting the DRD2/β‐catenin/ZEB1 signaling axis is a potentially promising therapeutic strategy for patients with CRC.

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Section: Discussionmentioning

confidence: 99%

Retracted: Overexpression of dopamine receptor D2 promotes colorectal cancer progression by activating the β‐catenin/ZEB1 axis

Lee¹,

Shim²,

Kong

et al. 2021

Cancer Science

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“…The Frizzled family, a distinct group within the superfamily of G protein-coupled receptors, consists of ten different seven-transmembrane receptors groups, divided into four clusters based on their amino-acid composition. FZD10 protein is a cell surface receptor, which is activated by Wnt proteins and involved in the regulation of cellular function [10,11,12,13,14,15] and belongs to the cluster 3, along with FZD4 and FZD9 [16]. We proved that the modulation of the FZD10 expression level in small EVs strongly depends on the stage of disease, and that, consequently, the evolution of pathology can be monitored by evaluating the level of protein expression therein [8].…”

Section: Introductionmentioning

confidence: 99%

FZD10 Carried by Exosomes Sustains Cancer Cell Proliferation

Scavo

Depalo

Rizzi

et al. 2019

Cells

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Extracellular vesicles (EVs) are involved in intercellular communication during carcinogenesis, and cancer cells are able to secrete EVs, in particular exosomes containing molecules, that can be transferred to recipient cells to induce pathological processes and significant modifications, as metastasis, increase of proliferation, and carcinogenesis evolution. FZD proteins, a family of receptors comprised in the Wnt signaling pathway, play an important role in carcinogenesis of the gastroenteric tract. Here, a still unknown role of Frizzled 10 (FZD10) protein was identified. In particular, the presence of FZD10 and FZD10-mRNA in exosomes extracted from culture medium of the untreated colorectal, gastric, hepatic, and cholangio cancer cell lines, was detected. A substantial reduction in the FZD10 and FZD10-mRNA level was achieved in FZD10-mRNA silenced cells and in their corresponding exosomes. Concomitantly, a significant decrease in viability of the silenced cells compared to their respective controls was observed. Notably, the incubation of silenced cells with the exosomes extracted from culture medium of the same untreated cells promoted the restoration of the cell viability and, also, of the FZD10 and FZD10-mRNA level, thus indicating that the FZD10 and FZD10-mRNA delivering exosomes may be potential messengers of cancer reactivation and play an active role in long-distance metastatization.

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“…Being a cell surface receptor, their activation mediate downstream molecular signaling cascades leading to the regulation of cellular functions. Studies on GPCR-associated tumorigenesis have further revealed the role of GPCRs as a “cancer driver” during tumor development [2,3,4,5,6]. The GPCRs comprise the largest class of membranous proteins in the human genome.…”

Section: Introductionmentioning

confidence: 99%

Deregulation of Frizzled Receptors in Hepatocellular Carcinoma

Chan

2018

IJMS

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G protein-coupled receptors (GPCRs) have a substantial role in tumorigenesis and are described as a “cancer driver”. Aberrant expression or activation of GPCRs leads to the deregulation of downstream signaling pathways, thereby promoting cancer progression. In hepatocellular carcinoma (HCC), the Wnt signaling pathway is frequently activated and it is associated with an aggressive HCC phenotype. Frizzled (FZD) receptors, a family member of GPCRs, are known to mediate Wnt signaling. Accumulating findings have revealed the deregulation of FZD receptors in HCC and their functional roles have been implicated in HCC progression. Given the important role of FZD receptors in HCC, we summarize here the expression pattern of FZD receptors in HCC and their corresponding functional roles during HCC progression. We also further review and highlight the potential targeting of FZD receptors as an alternative therapeutic strategy in HCC.

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Cancer driver G-protein coupled receptor (GPCR) induced β-catenin nuclear localization: the transcriptional junction

Cited by 13 publications

References 105 publications

Retracted: Overexpression of dopamine receptor D2 promotes colorectal cancer progression by activating the β‐catenin/ZEB1 axis

Retracted: Overexpression of dopamine receptor D2 promotes colorectal cancer progression by activating the β‐catenin/ZEB1 axis

FZD10 Carried by Exosomes Sustains Cancer Cell Proliferation

Deregulation of Frizzled Receptors in Hepatocellular Carcinoma

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