c-Jun Induces Mammary Epithelial Cellular Invasion and Breast Cancer Stem Cell Expansion

“…cJun may be an intermediate. When overexpressed in response to ERBB2 in mammary gland, it induces both invasion and mammosphere growth (Jiao et al, 2010).…”

Section: Cancer Cells S Floor Et Almentioning

confidence: 99%

Cancer cells in epithelial-to-mesenchymal transition and tumor-propagating–cancer stem cells: distinct, overlapping or same populations

Floor¹,

Staveren²,

et al. 2011

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“…Many studies have demonstrated that altered CCL5 expression in patients with breast tumors, melanoma, lung, prostate, cervical and pancreatic cancer is significantly correlated with disease progression, poor prognosis and tumor cell chemotherapy resistance (4-7). CCL5 can be expressed and secreted either by tumors themselves or by the tumor microenvironment stromal cells and substantially promotes the resistance of ovarian cancer cells to cisplatin (8,9). However, the role of CCL5 and the mechanisms underlying cisplatin resistance in ovarian cancers have not yet been fully clarified.…”

Section: Introductionmentioning

confidence: 99%

Cisplatin-induced CCL5 secretion from CAFs promotes cisplatin-resistance in ovarian cancer via regulation of the STAT3 and PI3K/Akt signaling pathways

Zhou

Sun

et al. 2016

International Journal of Oncology

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Abstract. Currently, acquired resistance to cisplatin (DDP) is a substantial obstacle to reducing the morbidity and mortality due to ovarian malignant tumors. Nevertheless, cisplatin plays a vital role in killing the tumor cells while it may also be a 'primer' involved in chemotherapy resistance. We found that the cisplatin-induced chemokine (C-C motif) ligand 5 (CCL5) secretion derived from cancer-associated fibroblasts (CAFs) promoted ovarian cancer cell resistance to cisplatin. Via a cytokine chip assay, we identified a spectrum of secreted proteins that were derived from the CAFs through cisplatin-induced treatment. Among these, CCL5 significantly attenuated the cytotoxic effect of cisplatin chemotherapy in vitro and in vivo. Additionally, CCL5 expression was also detected in 62 serous ovarian cancer patient tissue specimens using IHC, and the results demonstrated that chemotherapy resistant patients displayed higher expression of CCL5 than the chemo-sensitive patients (P<0.05). Mechanistically, we found that CCL5 notably increased STAT3 and Akt phosphorylation levels in ovarian cancer cells. These results indicated that cisplatininduced CCL5 secretion derived from the CAFs may promote cisplatin resistance, which was mediated by regulation of the STAT3 and PI3K/Akt signal pathways.

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“…Murooka and colleagues reported that in CCR5-transfected MCF-7 cells, CCL5 promotes proliferation and survival in an mTOR-dependent manner (18). Autocrine secretion of CCL5 controls migration and invasiveness of human breast cancer cells in vitro (12,19). Forced expression of CCL5 increased tumor metastasis approximately 1.8-fold in one study of MDA-MB-231 cells but had no effect in the 168 breast cancer cell line (13,20).…”

Section: Introductionmentioning

confidence: 99%

“…CCL5 can be expressed and secreted either by breast cancer cells (9)(10)(11)(12) or by nonmalignant stromal cells at the primary or metastatic sites (13). However, the roles of CCL5 and its receptors in breast cancer are not fully understood.…”

Section: Introductionmentioning

confidence: 99%

CCR5 Antagonist Blocks Metastasis of Basal Breast Cancer Cells

et al. 2012

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The roles of the chemokine CCL5 and its receptor CCR5 in breast cancer progression remain unclear. Here, we conducted microarray analysis on 2,254 human breast cancer specimens and found increased expression of CCL5 and its receptor CCR5, but not CCR3, in the basal and HER-2 genetic subtypes. The subpopulation of human breast cancer cell lines found to express CCR5 displayed a functional response to CCL5. In addition, oncogene transformation induced CCR5 expression, and the subpopulation of cells that expressed functional CCR5 also displayed increased invasiveness. The CCR5 antagonists maraviroc or vicriviroc, developed to block CCR5 HIV coreceptor function, reduced in vitro invasion of basal breast cancer cells without affecting cell proliferation or viability, and maraviroc decreased pulmonary metastasis in a preclinical mouse model of breast cancer. Taken together, our findings provide evidence for the key role of CCL5/CCR5 in the invasiveness of basal breast cancer cells and suggest that CCR5 antagonists may be used as an adjuvant therapy to reduce the risk of metastasis in patients with the basal breast cancer subtype. Cancer Res; 72(15); 3839-50. Ó2012 AACR.

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c-Jun Induces Mammary Epithelial Cellular Invasion and Breast Cancer Stem Cell Expansion

Cited by 129 publications

References 52 publications

Cancer cells in epithelial-to-mesenchymal transition and tumor-propagating–cancer stem cells: distinct, overlapping or same populations

Cancer cells in epithelial-to-mesenchymal transition and tumor-propagating–cancer stem cells: distinct, overlapping or same populations

Cisplatin-induced CCL5 secretion from CAFs promotes cisplatin-resistance in ovarian cancer via regulation of the STAT3 and PI3K/Akt signaling pathways

CCR5 Antagonist Blocks Metastasis of Basal Breast Cancer Cells

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