Further evidence to support the melanocytic origin of MDA-MB-435

Ellison, Gillian; Klinowska, Teresa; Westwood, Russell; Docter, E; French, T.; Fox, J C

doi:10.1136/mp.55.5.294

Cited by 150 publications

(119 citation statements)

References 16 publications

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“…The lack of both CXCR4 and CXCL12 expression by the MDA-MB-435s cell line may reflect their clarification not as mammary carcinoma cells but as melanoma cells (Ellison et al, 2002). Thus, the expression profile acquired during mammary epithelial transformation was characteristically similar to highly migratory leukocytes in that CXCR4 expression predominates over little if any CXCL12 expression (Kimura et al, 2003).…”

Section: Loss Of Cxcl12 Expression In Mammary Carcinomamentioning

confidence: 98%

Epigenetic silencing of CXCL12 increases the metastatic potential of mammary carcinoma cells

2007

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Expression of the chemokine receptor CXCR4 has been linked with increased metastasis and decreased clinical prognosis in breast cancer. The current paradigm dictates that CXCR4 fosters carcinoma cell metastasis along a chemotactic gradient to organs expressing the ligand CXCL12. The present study asked if alterations in autocrine CXCR4 signaling via dysregulation of CXCL12 in mammary carcinoma cells modulated their metastatic potential. While CXCR4 was consistently detected, expression of CXCL12 characteristic of human mammary epithelium was silenced by promoter hypermethylation in breast cancer cell lines and primary mammary tumors. Stable re-expression of functional CXCL12 in ligand null cells increased orthotopic primary tumor growth in the mammary fat-pad model of tumorigenesis. Those data parallel increased carcinoma cell proliferation measured in vitro with little-to-no-impact on apoptosis. Moreover, re-expression of autocrine CXCL12 markedly reduced metastatic lung invasion assessed using in vivo bioluminescence imaging following tail vein injection. Consistent with those data, decreased metastasis reflected diminished intracellular calcium signaling and chemotactic migration in response to exogenous CXCL12 independent of changes in CXCR4 expression. Together these data suggest that an elevated migratory signaling response to ectopic CXCL12 contributes to the metastatic potential of CXCR4-expressing mammary carcinoma cells, subsequent to epigenetic silencing of autocrine CXCL12.

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Section: Loss Of Cxcl12 Expression In Mammary Carcinomamentioning

confidence: 98%

Epigenetic silencing of CXCL12 increases the metastatic potential of mammary carcinoma cells

2007

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“…All cells were maintained in a humidified 5% CO 2 environment at 37°C. The tissue origin of the MDA-MB-435 cells has been under debate for a few years [21][22][23][24], it expresses milk lipids [25], does not metastasize from subcutaneous sites [26] and in fact, still remains one of the few available models of orthotopic metastasis of breast cancer in animal models.…”

Section: Cell Culturementioning

confidence: 99%

Epigenetic silencing contributes to the loss of BRMS1 expression in breast cancer

Metge

Frost

King

et al. 2008

Clin Exp Metastasis

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Breast Cancer Metastasis Suppressor 1 (BRMS1) suppresses metastasis of human breast cancer, ovarian cancer and melanoma in athymic mice. Studies have also shown that BRMS1 is significantly downregulated in some breast tumors, especially in metastatic disease. However, the mechanisms which regulate BRMS1 expression are currently unknown. Upon examination of the BRMS1 promoter region by methylation specific PCR (MSP) analysis, we discovered a CpG island (−3477 to −2214), which was found to be hypermethylated across breast cancer cell lines. A panel of 20 patient samples analyzed showed that 45% of the primary tumors and 60% of the matched lymph node metastases, displayed hypermethylation of BRMS1 promoter. Furthermore, we found a direct correlation between the methylation status of the BRMS1 promoter in the DNA isolated from tissues, with the loss of BRMS1 expression assessed by immunohistochemistry. There are several studies investigating the mechanism by which BRMS1 suppresses metastasis; however thus far there is no

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“…This cell line has widely been accepted as originating from a breast cancer, but some recent publications have suggested that the cells originate from a melanoma (Ellison et al, 2002). These cells and MCF-7 breast cancer cells were grown in monolayer cultures in RPMI 1640 medium (Gibco, Grand Island, NY) supplemented with 10% fetal calf serum, 20 mM HEPES buffer pH 7.5 and 2 mM L-glutamine (Gibco).…”

Section: Cell Culturementioning

confidence: 99%

Garlic arrests MDA-MB-435 cancer cells in mitosis, phosphorylates the proapoptotic BH3-only protein BimEL and induces apoptosis

et al. 2005

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Components of garlic (Allium sativum) can cause disruption of microtubules, cell cycle arrest, and apoptosis in cancer cells. We show here that a water-soluble extract of garlic arrested MDA-MB-435 cancer cells in mitosis and caused apoptosis. The proapoptotic BH3-only, bcl-2 family protein Bim EL , which in healthy cells can be tightly sequestered to the microtubule-associated dynein motor complex, was modified after garlic treatment. The main effect of garlic on Bim EL was a considerable increase in a phosphorylated form of the protein. This phosphorylation(s), probably partly dependent on c-jun N-terminal kinase activity, promoted mitochondrial localisation of Bim EL . Furthermore, inhibition of extracellular signal-regulated kinases 1/2 increased the amount of another form of Bim EL present in the mitochondrial cellular fraction. Treatment of cells with the garlic compound diallyl disulphide had similar effects on Bim EL . The results indicate that the apoptotic effect of garlic and a combination of garlic and the inhibitor of extracellular signalregulated kinases 1/2 in MDA-MB-435 cells partly is due to modifications that are necessary for translocation of the proapoptotic protein Bim EL to mitochondria where it executes its proapoptotic function.

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Further evidence to support the melanocytic origin of MDA-MB-435

Cited by 150 publications

References 16 publications

Epigenetic silencing of CXCL12 increases the metastatic potential of mammary carcinoma cells

Epigenetic silencing of CXCL12 increases the metastatic potential of mammary carcinoma cells

Epigenetic silencing contributes to the loss of BRMS1 expression in breast cancer

Garlic arrests MDA-MB-435 cancer cells in mitosis, phosphorylates the proapoptotic BH3-only protein BimEL and induces apoptosis

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