Irradiation of normal mouse tissue increases the invasiveness of mammary cancer cells

Lemay, Rosalie; Archambault, Mélanie; Tremblay, Luc; Bujold, Rachel; Lepage, Martin; Paquette, Benoît

doi:10.3109/09553002.2011.542541

Cited by 21 publications

(15 citation statements)

References 37 publications

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“…Multiple RIBEs, including cell growth stimulation, DNA damage, and cell death, have been observed in tumour cells in vitro (Shao et al , 2003a, 2003c; Gow et al , 2010). Using mouse model, the bystander responses of internal tumour cells or tissues were also confirmed in vivo , and cancer-associated events, such as p 53 alteration, MMPs activity, and epigenetic change, were proved to be involved in the RIBE (Camphausen et al , 2003; Koturbash et al , 2007; Lemay et al , 2011). …”

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confidence: 91%

Cytochrome-c mediated a bystander response dependent on inducible nitric oxide synthase in irradiated hepatoma cells

Ren

et al. 2012

Br J Cancer

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Background:Radiation-induced bystander effect (RIBE) has important implication in tumour radiotherapy, but the bystander signals are still not well known.Methods:The role of cytochrome-c (cyt-c) and free radicals in RIBE on human hepatoma cells HepG2 was investigated by detecting the formation of bystander micronuclei (MN) and the generation of endogenous cyt-c, inducible nitric oxide (NO) synthase (iNOS), NO, and reactive oxygen species (ROS) molecules.Results:When HepG2 cells were cocultured with an equal number of irradiated HepG2 cells, the yield of MN in the nonirradiated bystander cells was increased in a manner depended on radiation dose and cell coculture time, but it was diminished when the cells were treated with cyclosporin A (CsA), an inhibitor of cyt-c release. Meanwhile the CsA treatment inhibited radiation-induced NO but not ROS. Both of the depressed bystander effect and NO generation in the CsA-treated cells were reversed when 5 μ cyt-c was added in the cell coculture medium. But these exogenous cyt-c-mediated overproductions of NO and bystander MN were abolished when the cells were pretreated with s-methylisothiourea sulphate, an iNOS inhibitor.Conclusion:Radiation-induced cyt-c has a profound role in regulating bystander response through an iNOS-triggered NO signal but not ROS in HepG2 cells.

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confidence: 91%

Cytochrome-c mediated a bystander response dependent on inducible nitric oxide synthase in irradiated hepatoma cells

Ren

et al. 2012

Br J Cancer

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“…This radiation-enhancement of cancer cell invasion was associated with an increase in COX-2 and MMP-2 expression (Lemay et al , 2011; Paquette et al , 2008). It remains to be determined whether a COX-2 inhibitor administrated in an animal model would prevent radiation-enhancement of cancer cell invasion.…”

Section: Discussionmentioning

confidence: 99%

Radiation-enhancement of MDA-MB-231 breast cancer cell invasion prevented by a cyclooxygenase-2 inhibitor

et al. 2011

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Background:Recent evidences support that radiation can promote the invasion of cancer cells. As interactions between cancer cells and surrounding stromal cells can have an important role in tumour progression, we determined whether an irradiation to fibroblasts can enhance the invasiveness of breast cancer cells. The role of cyclooxygenase-2 (COX-2), an inflammatory enzyme frequently induced by radiotherapy, was investigated.Methods:Irradiated 3T3 fibroblasts were plated in the lower compartment of invasion chambers and used as chemoattractant for non-irradiated human breast cancer cell MDA-MB-231, which are oestrogen receptor negative (ER(−)) and the oestrogen receptor positive (ER(+)) MCF-7 cells. Stimulation of COX-2 expression in irradiated 3T3 cells was measured by a semi-quantitative qPCR and western blot. Capacity of the major product of COX-2, the prostaglandin E2 (PGE2), to stimulate the production of the matrix metalloproteinase-2 (MMP-2) and cancer cell invasion were assessed with a zymography gel and invasion chambers.Results:Irradiation (5 Gy) of 3T3 fibroblasts increased COX-2 expression and enhanced by 5.8-fold the invasiveness of non-irradiated MDA-MB-231 cells, while their migration was not modified. Addition of the COX-2 inhibitor NS-398 completely prevented radiation-enhancement of cancer cell invasion. Further supporting the potential role of COX-2, addition of PGE2 has increased cancer cell invasion and release of MMP-2 from the MDA-MB-231 cells. This effect of radiation was dependant on the expression of membrane type 1 (MT1)–MMP, which is required to activate the MMP-2, but was not associated with the ER status. Although irradiated fibroblasts stimulated the invasiveness of MDA-MB-231 ER(−) cells, no enhancement was measured with the ER(+) cell line MCF-7.Conclusions:Radiation-enhancement of breast cancer cell invasion induced by irradiated 3T3 fibroblasts is not dependant on the ER status, but rather the expression of MT1–MMP. This adverse effect of radiation can be prevented by a specific COX-2 inhibitor.

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“…The research group of Dr. Paquette of Sherbrooke University has studied whether irradiation of normal tissues could increase the invasiveness of breast cancer cells in a mouse model. They concluded that the implantation of non-irradiated mammary cancer cells in previously irradiated normal tissue enhanced the invasive capacity of the mammary cancer cells (Lemay et al, 2011). Another hypothesis from the same group is that there is an activation of transforming growth factor beta (TGF-β) from healthy tissues by radiation.…”

Section: Breast Cancermentioning

confidence: 99%

“…The tube containing the mouse was positioned in relation to a mark onto the stereotactic frame. The use of this device is reported by Lemay et al in 2011(Lemay et al, 2011. In a long-term project that uses several animals, Charest et al developed in 2009 a stereotactic frame for rat that allows constant and reproducible positioning using the same target coordinates (Charest et al, 2009).…”

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confidence: 99%

Applications of Gamma Knife Radiosurgery for Experimental Investigations in Small Animal Models

Charest¹,

Paquette²,

Mathieu³

2011

Gamma Knife Radiosurgery

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Irradiation of normal mouse tissue increases the invasiveness of mammary cancer cells

Abstract: Implantation of non-irradiated mammary cancer cells in previously irradiated normal tissue enhances the invasive capacity of the mammary cancer cells and is associated with an increased activity of MMP-2 and -9 in the irradiated normal tissue.

Cited by 21 publications

References 37 publications

Cytochrome-c mediated a bystander response dependent on inducible nitric oxide synthase in irradiated hepatoma cells

Cytochrome-c mediated a bystander response dependent on inducible nitric oxide synthase in irradiated hepatoma cells

Radiation-enhancement of MDA-MB-231 breast cancer cell invasion prevented by a cyclooxygenase-2 inhibitor

Applications of Gamma Knife Radiosurgery for Experimental Investigations in Small Animal Models

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