CXCR7 in tumorigenesis and progression

Hou, Kailin; Hao, Ming-Gang; Bo, Juan-jie; Wang, Jianhua

doi:10.5732/cjc.009.10404

Cited by 19 publications

(19 citation statements)

References 27 publications

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“…Interestingly, down-regulation of Lipocalin2 (LCN2), a marker for kidney injury (Viau et al, 2010), implicated in kidney epithelial cell morphogenesis (Gwira et al, 2005) and previously shown to be dysregulated in Apc Min/+ intestinal adenomas (Reichling et al, 2005), was observed in the APC shRNA MDCK cells. Other dysregulated genes including the alpha 1 subunit of type IV collagen (COL4A1, a basement membrane component), C-X-C chemokine receptor type 7 (CXCR7), and ADAM metallopeptidase with thrombospondin type 1, motif 6 (ADAMTS6), are implicated in controlling cell-cell or cell-matrix interactions (Kuhn, 1995; Bevitt et al, 2005; Hou et al, 2010; Aikio et al, 2012). These data collectively support a model in which APC loss-of-function in epithelial cells (through mutation and deletion of its c-terminus or gene silencing) leads to loss of polarity and tissue architecture, and subsequent tumor initiation, via altered communication between neighboring cells and the substratum.…”

Section: Resultsmentioning

confidence: 99%

The APC tumor suppressor is required for epithelial cell polarization and three-dimensional morphogenesis

Lesko

Goss

Yang

et al. 2015

Biochimica et Biophysica Acta (BBA) - Molecular Cell Research

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The Adenomatous Polyposis Coli (APC) tumor suppressor has been previously implicated in the control of apical-basal polarity; yet, the consequence of APC loss-of-function in epithelial polarization and morphogenesis has not been characterized. To test the hypothesis that APC is required for the establishment of normal epithelial polarity and morphogenesis programs, we generated APC-knockdown epithelial cell lines. APC depletion resulted in loss of polarity and multi-layering on permeable supports, and enlarged, filled spheroids with disrupted polarity in 3D culture. Importantly, these effects of APC knockdown were independent of Wnt/β-catenin signaling, but were rescued with either full-length or a carboxy (c)-terminal segment of APC. Moreover, we identified a gene expression signature associated with APC knockdown that points to several candidates known to regulate cell-cell and cell-matrix communication. Analysis of epithelial tissues from mice and humans carrying heterozygous APC mutations further support the importance of APC as a regulator of epithelial behavior and tissue architecture. These data also suggest that the initiation of epithelial-derived tumors as a result of APC mutation or gene silencing may be driven by loss of polarity and dysmorphogenesis.

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Section: Resultsmentioning

confidence: 99%

The APC tumor suppressor is required for epithelial cell polarization and three-dimensional morphogenesis

Lesko

Goss

Yang

et al. 2015

Biochimica et Biophysica Acta (BBA) - Molecular Cell Research

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“…Depending on the origin of cancer, CXCR7 was described to be expressed both by the tumour cells and the stromal cells (Hou et al , 2010; Sun et al , 2010). Little is known about the protein expression of CXCR7 in CRC.…”

Section: Resultsmentioning

confidence: 99%

“…The CXCR7/CXCR7 ligands axis might be directly implicated in the tumour angiogenesis but also indirectly, by regulating processes that lead up to the expression of proangiogenic factors such as CXCL8 and VEGF (Wang et al , 2008; Hou et al , 2010). Therefore, we assessed the mRNA expression of CXCL8 and VEGF in HT29-injected mice treated (or not) with a CXCR7 antagonist.…”

Section: Resultsmentioning

confidence: 99%

“…The CXCR7 axis is known to be indirectly implicated in tumour vascularisation through processes leading up to the expression of proangiogenic factors such as CXCL8 and VEGF (Wang et al , 2008; Hou et al , 2010). In our study, we observed that in the lung metastases of CRC, CXCR7 axis failed to regulate the expression of CXCL8 and VEGF (at the level of transcription), rather suggesting a direct control of CXCR7 axis on vascular tumour growth.…”

Section: Discussionmentioning

confidence: 99%

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CXCR7 receptors facilitate the progression of colon carcinoma within lung not within liver

et al. 2012

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Background:Liver and lung metastases are the predominant cause of colorectal cancer (CRC)-related mortality. Chemokine-receptor pairs have a critical role in determining the metastatic progression of tumours. Our hypothesis was that disruption of CXCR7/CXCR7 ligands axis could lead to a decrease in CRC metastases.Methods:Primary tumours and metastatic tissues from patients with CRC were tested for the expression of CXCR7 and its ligands. Relevance of CXCR7/CXCR7 ligands for CRC metastasis was then investigated in mice using small pharmacological CXCR7 antagonists and CRC cell lines of human and murine origins, which – injected into mice – enable the development of lung and liver metastases.Results:Following injection of CRC cells, mice treated daily with CXCR7 antagonists exhibited a significant reduction in lung metastases. However, CXCR7 antagonists failed to reduce the extent of liver metastasis. Moreover, there were subtle differences in the expression of CXCR7 and its ligands between lung and liver metastases.Conclusion:Our study suggests that the activation of CXCR7 on tumour blood vessels by its ligands may facilitate the progression of CRC within lung but not within liver. Moreover, we provide evidence that targeting the CXCR7 axis may be beneficial to limit metastasis from colon cancer within the lungs.

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“…The role of CXCR7 has been identified by studies in malignant cells of various tumor types, including breast, lung, prostate and colorectal cancer, highlighting the role of CXCR7 in cancer growth, survival, adhesion, invasion and metastasis [19]. Miao et al [10] showed that CXCR7 promotes the tumor growth of breast and lung cancer cells and lung metastases in both immunodeficient and immunocompetent mouse models.…”

Section: Discussionmentioning

confidence: 99%

High expression of CXCR4, CXCR7 and SDF-1 predicts poor survival in renal cell carcinoma

et al. 2012

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BackgroundChemokines and their receptors are known to play important roles in the tumorigenesis of many malignancies. The aim of this study was to evaluate the prognostic impact of the expression of the chemokine SDF-1 and its receptors CXCR4 and CXCR7 in patients with renal cell carcinoma.MethodsThe expression of CXCR4, CXCR7 and SDF-1 in specimens from 97 renal cell carcinoma patients was evaluated by immunohistochemistry on a tissue microarray. These results were correlated with the clinicopathological parameters and survival of the patients.ResultsCXCR4 and CXCR7 were expressed in all patients, whereas SDF-1 was expressed in 61 patients (62.9%). No association was observed between the expression of CXCR4, CXCR7 or SDF-1 and the clinical or pathological data except between SDF-1 expression and Fuhrman’s grade (P = 0.015). Patients with high expression of CXCR4, CXCR7 and SDF-1 had shorter overall survival and recurrence-free survival than those with low expression. In a multivariate analysis, the high expression of CXCR4, CXCR7 and SDF-1 correlated with poor overall survival and recurrence-free survival independent of gender, age, AJCC stage, lymph node status, metastasis, histologic variant and Fuhrman’s grade.ConclusionsHigh levels of CXCR4, CXCR7 and SDF-1 were associated with poor overall survival and recurrence-free survival in renal cell carcinoma patients. CXCR4, CXCR7 and SDF-1 may serve as useful prognostic markers and therapeutic targets for renal cell carcinoma.

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CXCR7 in tumorigenesis and progression

Cited by 19 publications

References 27 publications

The APC tumor suppressor is required for epithelial cell polarization and three-dimensional morphogenesis

The APC tumor suppressor is required for epithelial cell polarization and three-dimensional morphogenesis

CXCR7 receptors facilitate the progression of colon carcinoma within lung not within liver

High expression of CXCR4, CXCR7 and SDF-1 predicts poor survival in renal cell carcinoma

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