Up-regulation of CXC chemokines and their receptors: implications for proinflammatory microenvironments of ovarian carcinomas and endometriosis

Furuya, Mitsuko; Suyama, Takahito; Usui, Hirokazu; Kasuya, Yoshitoshi; Nishiyama, Mariko; Tanaka, Naotake; Ishiwata, Isamu; Nagai, Yuichiro; Shozu, Makio; Kimura, Sadao

doi:10.1016/j.humpath.2007.03.023

Cited by 93 publications

(70 citation statements)

References 33 publications

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“…Similar to the expression of CXCL9 and CXCL10 ligands, increased expression of CXCR3 has been reported on the surface of EOC cells (Furuya et al 2007) and clear cell ovarian cancer cells (Furuya et al 2011). CXCR3 has been found to be expressed by endothelial cells while undergoing G 2 M and late S phases of the cell cycle (Romagnani et al 2001).…”

Section: Angiostatic Chemokine Ligands: Cxcl9 and Cxcl10 Expression Cmentioning

confidence: 70%

“…Primary ovarian cancer cells stimulated with IL17 and IFN-g can be induced to secrete CXCL9 and CXCL10 (Kryczek et al 2009), while CXCL11 (and CXCL9) expression has been detected in serous ovarian carcinoma cell lines and tissue by immunohistochemistry and reverse transcriptase PCR (Furuya et al 2007). These CXCR3-binding chemokines can inhibit endothelial cell migration and proliferation, attract cells involved in innate and adaptive immunity and increase MHC class I processing by tumour cells, thereby enhancing recognition by the immune system (Groom & Luster 2011, Wilke et al 2011; Fig.…”

Section: Angiostatic Chemokine Ligands: Cxcl9 and Cxcl10 Expression Cmentioning

confidence: 99%

“…CXC-mediated regulation of the EOC microenvironment appears to be primarily due to CXCL9 and CXCL10; the anti-tumour effect of CXCL11 in EOC is reportedly less efficient in mounting an anti-tumour response (Lasagni et al 2003, Furuya et al 2007). Similar to the expression of CXCL9 and CXCL10 ligands, increased expression of CXCR3 has been reported on the surface of EOC cells (Furuya et al 2007) and clear cell ovarian cancer cells (Furuya et al 2011).…”

Section: Angiostatic Chemokine Ligands: Cxcl9 and Cxcl10 Expression Cmentioning

confidence: 99%

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The emerging role of CXC chemokines in epithelial ovarian cancer

et al. 2012

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In recent years, chemokines have generated intense investigations due to their involvement in both physiological and pathological processes of inflammation, particularly in ovarian biology. The physiological process of ovulation in the normal ovary involves various chemokines that mediate the healing of the ruptured endometrium. It is now being reported that many of these chemokines are also associated with the cancer of the ovary. Chronic inflammation underlies the progression of ovarian cancer; therefore, it raises the possibility that chemokines are involved in the inflammatory process and mediate immune responses that may favour or inhibit tumour progression. Ovarian cancer is a gynaecological cancer responsible for highest rate of mortality in women. Although there have been several investigations and advances in surgery and chemotherapy, the survival rate for this disease remains low. This is mainly because of a lack of specific symptoms and biomarkers for detection. In this review, we have discussed the emerging role of the CXC chemokines in epithelial ovarian cancer (EOC). The CXC group of chemokines is gaining importance in the field of ovarian cancer for being angiostatic and angiogenic in function. While there have been several studies on the angiogenesis function, emerging research shows that ELR K CXC chemokines, CXCL9 and CXCL10, are angiostatic. Importantly, the angiostatic chemokines can inhibit the progression of EOC. Given that there are currently no biomarkers or specific therapeutic targets for the disease, these chemokines are emerging as promising targets for therapy.

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Section: Angiostatic Chemokine Ligands: Cxcl9 and Cxcl10 Expression Cmentioning

confidence: 70%

Section: Angiostatic Chemokine Ligands: Cxcl9 and Cxcl10 Expression Cmentioning

confidence: 99%

Section: Angiostatic Chemokine Ligands: Cxcl9 and Cxcl10 Expression Cmentioning

confidence: 99%

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The emerging role of CXC chemokines in epithelial ovarian cancer

et al. 2012

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“…Another laboratory has also shown that CXCR3 was detected in 32% of human melanomas examined and was associated with tumor thickness, absent lymphocyte infiltration, and the presence of distant metastasis (23). CXCR3 has been identified in biopsies of ovarian and renal cell carcinomas (18,19). Two laboratories have described the expression of CXCR3 in colon cancer (22,24) and observed CXCR3 both in the cytoplasm and plasma membrane of malignant, but not normal, colonic epithelium.…”

Section: Discussionmentioning

confidence: 98%

CXCR3 expression is associated with poor survival in breast cancer and promotes metastasis in a murine model

Norsworthy²,

Kundu³

et al. 2009

Molecular Cancer Therapeutics

131

111

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Breast tumor cells express the chemokine receptor CXCR3, which binds the ligands CXCL9, CXCL10, and CXCL11. CXCR3 and other chemokine receptors may mediate tumor metastasis by supporting migration of tumor cells to sites of ligand expression including the lymph nodes, lungs, and bone marrow. We examined the relationship of CXCR3 expression to clinical outcome in 75 women diagnosed with early-stage breast cancer. We detected CXCR3 in malignant epithelium from all tumors. Twelve percent were weakly positive and 64% had moderate levels of CXCR3. Strong CXCR3-positive staining was observed in 24% of tumors. Kaplan-Meier survival curves showed that high CXCR3 expression was associated with poorer overall survival; the unadjusted hazard ratio was 1.56 and it was marginally significant (P = 0.07). When interactions between lymph node status and CXCR3 were considered, the adjusted hazard ratio for CXCR3 was 2.62 (P = 0.02) for women with nodenegative disease at diagnosis, whereas the hazard ratio for CXCR3 was not significant for those with node-positive disease. CXCR3 gene silencing inhibited lung colonization and spontaneous lung metastasis from mammary glandimplanted tumors in a murine model. The size or growth rate of the locally growing tumors was not affected. The antimetastatic effect of CXCR3 gene silencing was compromised in mice depleted of Natural Killer cells or with mutations in IFN-;, suggesting that the role of CXCR3 is not simply to mediate tumor cell trafficking. These studies support the continued examination of CXCR3 as a potential therapeutic target in patients with breast cancer. [Mol Cancer Ther 2009;8(3):490 -8]

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“…7 In addition, CXCR4 was identified in cancer stem cells including breast cancer, ovarian cancer, prostate cancer, neuroblastoma and rhabdomyosarcoma. [13][14][15][16][17] It is therefore likely that a similar regulatory principle as it is operative in homing of HSCs might be employed by cancer cells as part of their metastatic potential.…”

mentioning

confidence: 99%

Stem cells: the challenge and opportunities

Messner

2008

Bone Marrow Transplant

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Up-regulation of CXC chemokines and their receptors: implications for proinflammatory microenvironments of ovarian carcinomas and endometriosis

Cited by 93 publications

References 33 publications

The emerging role of CXC chemokines in epithelial ovarian cancer

The emerging role of CXC chemokines in epithelial ovarian cancer

CXCR3 expression is associated with poor survival in breast cancer and promotes metastasis in a murine model

Stem cells: the challenge and opportunities

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