The relevance of the chemokine receptor ACKR3/CXCR7 on CXCL12-mediated effects in cancers with a focus on virus-related cancers

Freitas, Christelle; Desnoyer, Aude; Meuris, Floriane; Bachelerie, Françoise; Balabanian, Karl; Machelon, Véronique

doi:10.1016/j.cytogfr.2014.04.006

Cited by 46 publications

(35 citation statements)

References 98 publications

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“…A completely different picture was found for ACKR3, which, when expressed by cancer cells, acts as a tumor promoter by directly inducing an intracellular signaling of proliferation and survival or modulating the signaling of CXCR4, the receptor with which it shares the ligand CXCL12. Contrary to the other ACKRs, ACKR3 is up-regulated on cancer cells and on tumor endothelial cells compared with healthy tissues, and its expression correlates with disease progression [65].…”

Section: Discussionmentioning

confidence: 96%

“…ACKR3 is constitutively ubiquitinated; after agonist binding, it is deubiquitinated, binds b-arrestin, and undergoes internalization. It then releases chemokines in early endosomes for degradation, releases b-arrestin, and binds ubiquitin again, which allows it to be recycled back to the cell surface [63][64][65][66]. The functional role of ACKR3 is not only the modulation of CXCL12 bioavailability by scavenging but also the modulation of CXCR4 expression and function.…”

Section: Ackr3/cxcr7mentioning

confidence: 99%

“…In the cancer context, ACKR3 was initially found expressed on many tumor cell lines and in endothelial cells associated with tumors [70]. ACKR3 is also expressed by different tumor types [65] and is often found up-regulated in tumor tissues compared with their healthy counterparts. Some mechanisms of ACKR3 regulation have been described, such as hypoxia, DNA methylation of the tumor suppressor gene hypermethylated in cancer 1, microRNA-430 and microRNA-101 [65].…”

Section: Ackr3/cxcr7mentioning

confidence: 99%

“…ACKR3 is also expressed by different tumor types [65] and is often found up-regulated in tumor tissues compared with their healthy counterparts. Some mechanisms of ACKR3 regulation have been described, such as hypoxia, DNA methylation of the tumor suppressor gene hypermethylated in cancer 1, microRNA-430 and microRNA-101 [65]. Different from the other ACKRs, ACKR3 expression by cancer cells, in most of the cases, promotes the tumorigenesis process affecting tumor cell growth, survival, and metastasis [71].…”

Section: Ackr3/cxcr7mentioning

confidence: 99%

See 3 more Smart Citations

Atypical chemokine receptors in cancer: friends or foes?

Massara

Bonavita

Mantovani

et al. 2016

Journal of Leukocyte Biology

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The chemokine system is a fundamental component of cancer-related inflammation involved in all stages of cancer development. It controls not only leukocyte infiltration in primary tumors but also angiogenesis, cancer cell proliferation, and migration to metastatic sites. Atypical chemokine receptors are a new, emerging class of regulators of the chemokine system. They control chemokine bioavailability by scavenging, transporting, or storing chemokines. They can also regulate the activity of canonical chemokine receptors with which they share the ligands by forming heterodimers or by modulating their expression levels or signaling activity. Here, we summarize recent results about the role of these receptors (atypical chemokine receptor 1/Duffy antigen receptor for chemokine, atypical chemokine receptor 2/D6, atypical chemokine receptor 3/CXC-chemokine receptor 7, and atypical chemokine receptor 4/CC-chemokine receptor-like 1) on the tumorigenesis process, indicating that their effects are strictly dependent on the cell type on which they are expressed and on their coexpression with other chemokine receptors. Indeed, atypical chemokine receptors inhibit tumor growth and progression through their activity as negative regulators of chemokine bioavailability, whereas, on the contrary, they can promote tumorigenesis when they regulate the signaling of other chemokine receptors, such as CXC-chemokine receptor 4. Thus, atypical chemokine receptors are key components of the regulatory network of inflammation and immunity in cancer and may have a major effect on anti-inflammatory and immunotherapeutic strategies.

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Section: Discussionmentioning

confidence: 96%

Section: Ackr3/cxcr7mentioning

confidence: 99%

Section: Ackr3/cxcr7mentioning

confidence: 99%

Section: Ackr3/cxcr7mentioning

confidence: 99%

See 2 more Smart Citations

Atypical chemokine receptors in cancer: friends or foes?

Massara

Bonavita

Mantovani

et al. 2016

Journal of Leukocyte Biology

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“…Recently, CXCR7 has been found to have higher binding affinity to CXCL12 than CXCR4 [15]. Therefore, we explored which receptor was involved in CXCL12-mediated anti-apoptotic function in cancer cells.…”

Section: Cxcr7 Is Associated With Cxcl12-mediated Anti-apoptosis Of Lmentioning

confidence: 99%

High-Expressed CXCR7 Contributes to CXCL12-Mediated Protection from Apoptosis in Lymphoma Cells

Xu¹,

Deng²

2016

J Mol Genet Med

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Viral genes may act as oncogenes and interact with intracellular proteins, which are related to oncogenesis and tumor growth. Autocrining CXCL12 in growing tumor tissue plays critical roles in modulating cell proliferation and survival through its receptor CXCR4 and CXCR7. Recently, a number of research reports indicated that CXCR7 displays high expression in many kinds of tumor tissues and cell lines and that high -expressed CXCR7 may be involved in cell survival and migration. To date, CXCR7's biological function and signaling in cancer pathogenesis is unclear. In this study, we first found there are higher expression of CXCR7 in both lymphocyte nodes and EBV positive lymphoma cell line IB4. The results further suggested that high-expressed CXCR7 plays a role in CXCL12 mediated anti-apoptosis and inhibition of CXCR7 through CXCR7 inhibitor CCX771 significantly attenuated the function of CXCL12 on anti-apoptosis. Furthermore, we observed that CXCR7 inhibitor directly reduced protection of endogenous CXCL12 from apoptosis in EBV positive lymphoma cell line. Finally, the results revealed that CXCL12 activated CXCR7 trafficking to membrane and interaction of CXCR7 and β-arrestin-2 during anti-apoptosis process. The study suggested that the high-expressed CXCR7 may have effect on anti-apoptosis and inhibitor of CXCR7 may become potential target for cancer therapy.

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Extracellular Ubiquitin: Role in Myocyte Apoptosis and Myocardial Remodeling

Scofield

Amin

Singh

et al. 2015

Comprehensive Physiology

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Ubiquitin (UB) is a highly conserved low molecular weight (8.5 kDa) protein. It consists of 76 amino acid residues and is found in all eukaryotic cells. The covalent linkage of UB to a variety of cellular proteins (ubiquitination) is one of the most common posttranslational modifications in eukaryotic cells. This modification generally regulates protein turnover and protects the cells from damaged or misfolded proteins. The polyubiquitination of proteins serves as a signal for degradation via the 26S proteasome pathway. UB is present in trace amounts in body fluids. Elevated levels of UB are described in the serum or plasma of patients under a variety of conditions. Extracellular UB is proposed to have pleiotropic roles including regulation of immune response, anti-inflammatory, and neuroprotective activities. CXCR4 is identified as receptor for extracellular UB in hematopoietic cells. Heart failure represents a major cause of morbidity and mortality in western society. Cardiac remodeling is a determinant of the clinical course of heart failure. The components involved in myocardial remodeling include-myocytes, fibroblasts, interstitium, and coronary vasculature. Increased sympathetic nerve activity in the form of norepinephrine is a common feature during heart failure. Acting via β-adrenergic receptor (β-AR), norepinephrine is shown to induce myocyte apoptosis and myocardial fibrosis. β-AR stimulation increases extracellular levels of UB in myocytes, and UB inhibits β-AR-stimulated increases in myocyte apoptosis and myocardial fibrosis. This review summarizes intracellular and extracellular functions of UB with particular emphasis on the role of extracellular UB in cardiac myocyte apoptosis and myocardial remodeling.

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The relevance of the chemokine receptor ACKR3/CXCR7 on CXCL12-mediated effects in cancers with a focus on virus-related cancers

Cited by 46 publications

References 98 publications

Atypical chemokine receptors in cancer: friends or foes?

Atypical chemokine receptors in cancer: friends or foes?

High-Expressed CXCR7 Contributes to CXCL12-Mediated Protection from Apoptosis in Lymphoma Cells

Extracellular Ubiquitin: Role in Myocyte Apoptosis and Myocardial Remodeling

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