Duffy antigen receptor for chemokines in laryngeal squamous cell carcinoma as a negative regulator

Sun, Guohua; Wang, Yu; Zhu, Yixin; Huang, Chenlu; Ji, Qinghai

doi:10.3109/00016489.2010.516012

Cited by 16 publications

(9 citation statements)

References 19 publications

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“…The present study suggested that DARC may inhibit EOC growth and metastasis via an anti-angiogenesis effect. This result is partially consistent with certain previous studies in other types of cancer, including non-small-cell lung cancer (26), breast cancer (13,31,32), thyroid cancer (20) and laryngeal squamous cell carcinoma (33). The inhibitory effect of DARC on ovarian cancer growth and metastasis is mainly due to its ability to sequester pro-malignant chemokines.…”

Section: Discussionsupporting

confidence: 93%

The expression of Duffy antigen receptor for chemokines by epithelial ovarian cancer decreases growth potential

Zhu

Jiang

2017

Oncology Letters

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Epithelial ovarian cancer (EOC) is one of the main causes of cancer-associated mortality in females with gynecological malignancies. Duffy antigen receptor for chemokines (DARC) has previously been reported to be involved in tumor growth and the inhibition of tumor metastasis. However, the association between DARC and EOC remains unknown. The aim of the present study was to investigate the expression of DARC in the SKOV3 human epithelial ovarian cancer cell line with the establishment of a subcutaneous model in nude mice. To investigate the effects of DARC on the tumorigenesis of human epithelial ovarian cancer cells, GV287-DARC-L.V lentiviral vectors containing a DARC overexpression construct were transfected into SKOV3 cells. The present study revealed that transfection with DARC reduced the viability of SKOV3 cells in vitro by performing an MTT assay. SKOV3-DARC and SKOV3-negative control (NC) cells cultured in vitro were injected into nude mice to establish a subcutaneous model. The ovarian tumor volumes and the tumor weights were observed. Immunohistochemistry to detect CD31 expression was used to determine the microvessel density (MVD) in SKOV3-DARC and SKOV3-NC tumors. The results of the present study revealed that DARC-induced inhibition of tumor growth was associated with MVD in xenograft tumors. This suggested that DARC was a negative regulator of tumor growth in EOC, primarily via the inhibition of tumor angiogenesis.

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Section: Discussionsupporting

confidence: 93%

The expression of Duffy antigen receptor for chemokines by epithelial ovarian cancer decreases growth potential

Zhu

Jiang

2017

Oncology Letters

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“…This finding is of particular interest given that a recent study of three populations of African descent found a relationship between a functional polymorphism in the DARC gene and an increased susceptibility to asthma (59). Moreover, in several types of cancer, increased DARC expression was associated with decreased tumor metastasis and tumor size, as well as higher survival rates (60,61). Our results indicate that the inhibitory effect of CXCL1 is mediated through DARC and suggest that DARC may play a protective role in migration-dependent diseases, such as asthma and cancer.…”

Section: Discussionmentioning

confidence: 87%

CXCL1 Inhibits Airway Smooth Muscle Cell Migration through the Decoy Receptor Duffy Antigen Receptor for Chemokines

Al-Alwan

Chang

Rousseau

et al. 2014

The Journal of Immunology

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Airway smooth muscle cell (ASMC) migration is an important mechanism postulated to play a role in airway remodeling in asthma. CXCL1 chemokine has been linked to tissue growth and metastasis. In this study, we present a detailed examination of the inhibitory effect of CXCL1 on human primary ASMC migration and the role of the decoy receptor, Duffy AgR for chemokines (DARC), in this inhibition. Western blots and pathway inhibitors showed that this phenomenon was mediated by activation of the ERK-1/2 MAPK pathway, but not p38 MAPK or PI3K, suggesting a biased selection in the signaling mechanism. Despite being known as a nonsignaling receptor, small interference RNA knockdown of DARC showed that ERK-1/2 MAPK activation was significantly dependent on DARC functionality, which, in turn, was dependent on the presence of heat shock protein 90 subunit α. Interestingly, DARC- or heat shock protein 90 subunit α–deficient ASMCs responded to CXCL1 stimulation by enhancing p38 MAPK activation and ASMC migration through the CXCR2 receptor. In conclusion, we demonstrated DARC’s ability to facilitate CXCL1 inhibition of ASMC migration through modulation of the ERK-1/2 MAPK–signaling pathway.

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“…A protective role of ACKR1 in cancer is also suggested by data obtained with different human tumors. In breast [29,34,35], thyroid [36], colorectal [37], and laryngeal squamous cell [38] tumors, ACKR1 expression was positively correlated with a better outcome, even if the cell types expressing ACKR1 in these samples were not characterized. In summary, these results indicate ACKR1 as a negative regulator of tumor growth.…”

Section: Ackr1/darcmentioning

confidence: 97%

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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Duffy antigen receptor for chemokines in laryngeal squamous cell carcinoma as a negative regulator

Cited by 16 publications

References 19 publications

The expression of Duffy antigen receptor for chemokines by epithelial ovarian cancer decreases growth potential

The expression of Duffy antigen receptor for chemokines by epithelial ovarian cancer decreases growth potential

CXCL1 Inhibits Airway Smooth Muscle Cell Migration through the Decoy Receptor Duffy Antigen Receptor for Chemokines

Atypical chemokine receptors in cancer: friends or foes?

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