The Role of CXCR7/RDC1 as a Chemokine Receptor for CXCL12/SDF-1 in Prostate Cancer

Wang, Jianhua; Shiozawa, Yusuke; Wang, Jincheng; Wang, Yu; Jung, Younghun; Pienta, Kenneth J.; Mehra, Rohit; Loberg, Robert D.; Taichman, Russell S.

doi:10.1074/jbc.m707465200

Cited by 418 publications

(459 citation statements)

References 50 publications

(45 reference statements)

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“…These reports suggested that CXCR7 may scavenge the CXCL12 in the stationary, nonmigrating cells. Prostate cancer cells expressing CXCR7 suggest a role for this receptor in adhesion, invasiveness, and survival, where activation of Akt is linked to CXCR7 and results in the regulation of a number of genes associated with the NF-κB and MAP kinase pathways (32). Our current data, in which CXCR7 is an active receptor capable of signaling through β-arrestin, provide a mechanistic basis for understanding these earlier studies.…”

Section: Discussionmentioning

confidence: 53%

β-arrestin- but not G protein-mediated signaling by the “decoy” receptor CXCR7

Rajagopal

Kim

Ahn

et al. 2009

Proc. Natl. Acad. Sci. U.S.A.

510

532

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Ubiquitously expressed seven-transmembrane receptors (7TMRs) classically signal through heterotrimeric G proteins and are commonly referred to as G protein-coupled receptors. It is now recognized that 7TMRs also signal through β-arrestins, which act as versatile adapters controlling receptor signaling, desensitization, and trafficking. Most endogenous receptors appear to signal in a balanced fashion using both β-arrestin and G protein-mediated pathways. Some 7TMRs are thought to be nonsignaling “decoys” because of their inability to activate typical G protein signaling pathways; it has been proposed that these receptors act to scavenge ligands or function as coreceptors. Here we demonstrate that ligand binding to the decoy receptor CXCR7 does not result in activation of signaling pathways typical of G proteins but does activate MAP kinases through β-arrestins in transiently transfected cells. Furthermore, we observe that vascular smooth muscle cells that endogenously express CXCR7 migrate to its ligand interferon-inducible T-cell alpha chemoattractant (ITAC), an effect that is significantly attenuated by treatment with either a CXCR7 antagonist or β-arrestin depletion by siRNA. This example of an endogenous “β-arrestin-biased” 7TMR that signals through β-arrestin in the absence of G protein activation demonstrates that some 7TMRs encoded in the genome have evolved to signal through β-arrestin exclusively and suggests that other receptors that are currently thought to be orphans or decoys may also signal through such nonclassical pathways.

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Section: Discussionmentioning

confidence: 53%

β-arrestin- but not G protein-mediated signaling by the “decoy” receptor CXCR7

Rajagopal

Kim

Ahn

et al. 2009

Proc. Natl. Acad. Sci. U.S.A.

510

532

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“…Stromal-derived factor-1 has been reported to be associated with the metastasis and progression of prostate cancer. 38 The ERb, originally isolated from rat prostate, has a variety of its isoforms, that is, splicing variants. Those isoforms are expressed in an organ-specific manner, but …”

Section: Discussionmentioning

confidence: 99%

Effect of selective estrogen receptor modulators on cell proliferation and estrogen receptor activities in normal human prostate stromal and epithelial cells

Nomura

Kawashima

Masaki

et al. 2009

Prostate Cancer Prostatic Dis

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We examined the effect of E 2 and selective estrogen receptor modulators (SERMs) on the proliferation and estrogen receptor (ER) activities in normal human prostate cells. SERMs such as toremifene, raloxifene and tamoxifen suppressed the proliferation of prostate epithelial and stromal cells whereas anti-androgens did not. In prostate stromal cells, the transactivation activities of ER were enhanced by adding E 2 and reduced remarkably by toremifene. The results indicate that the ER-mediated pathway plays a central role in the growth of normal prostate cells.

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“…CXCR7 is expressed in diverse cell types including malignant cells [98] as well as in tumor-associated blood vessels [99] . CXCR7-dependent signals promote the growth of breast and lung tumors, enhance lung metastasis and tumor aggressiveness in prostate cancer [99,100] . Antagonists of CXCR7 prevented tumor growth in animal models, hence validating this receptor as a potential target for the development of novel anti-cancer therapeutics [98] .…”

Section: Gpcrs Activated By Chemokinesmentioning

confidence: 99%

GPCRs and cancer

Lappano

2012

Acta Pharmacol Sin

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G-protein-coupled receptors (GPCRs), which represent the largest gene family in the human genome, play a crucial role in multiple physiological functions as well as in tumor growth and metastasis. For instance, various molecules like hormones, lipids, peptides and neurotransmitters exert their biological effects by binding to these seven-transmembrane receptors coupled to heterotrimeric G-proteins, which are highly specialized transducers able to modulate diverse signaling pathways. Furthermore, numerous responses mediated by GPCRs are not dependent on a single biochemical route, but result from the integration of an intricate network of transduction cascades involved in many physiological activities and tumor development. This review highlights the emerging information on the various responses mediated by a selected choice of GPCRs and the molecular mechanisms by which these receptors exert a primary action in cancer progression. These findings provide a broad overview on the biological activity elicited by GPCRs in tumor cells and contribute to the identification of novel pharmacological approaches for cancer patients.

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The Role of CXCR7/RDC1 as a Chemokine Receptor for CXCL12/SDF-1 in Prostate Cancer

Cited by 418 publications

References 50 publications

β-arrestin- but not G protein-mediated signaling by the “decoy” receptor CXCR7

β-arrestin- but not G protein-mediated signaling by the “decoy” receptor CXCR7

Effect of selective estrogen receptor modulators on cell proliferation and estrogen receptor activities in normal human prostate stromal and epithelial cells

GPCRs and cancer

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