Radiation-induced lung damage promotes breast cancer lung-metastasis through CXCR4 signaling

Feys, Lynn; Descamps, Benedicte; Vanhove, Christian; Vral, Anne; Veldeman, Liv; Vermeulen, Stefan; Wagter, Carlos De; Bracke, Marc; Wever, Olivier De

doi:10.18632/oncotarget.5666

Cited by 43 publications

(43 citation statements)

References 61 publications

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“…Paquette et al (2007) showed that 20Gy irradiation of basement membrane components in an invasion assay led to increased invasion of MDA-MB-231 breast cancer cells through upregulation of several matrix metalloproteinases (MMP-2, MT1-MMP, and TIMP-2) [98]. An increase in invasive capacity following radiation, mediated through matrix metalloproteinase expression, has also been reported in a number of other cancer cells types, including melanoma [92], pancreatic cancer [99,100], glioma [101][102][103], rectal carcinoma [104], colon carcinoma, and osteosarcoma [105]. There is also evidence that irradiated cancer cells may secrete chemotactic factors that enhance the migration of neighbouring cells [106].…”

Section: The Effect Of Radiation On Cancer Cell Motility Invasion Amentioning

confidence: 98%

“…Hypoxia stimulates angiogenesis and this will enhance both tumour growth, by re-establishing neovasculature, and metastasis, as briefly described previously. Enhanced establishment of lung metastases, for example, has been reported in a breast cancer mouse model following a single therapeutic dose of radiation to the thorax of the animals [92]. The reason for these effects seems to be that cancer cells damaged or killed by radiation secrete a range of soluble factors that stimulate angiogenesis and enhance cancer cell migration and invasion [93,94].…”

Section: The Effect Of Radiation On Angiogenesismentioning

confidence: 99%

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Does Direct and Indirect Exposure to Ionising Radiation Influence the Metastatic Potential of Breast Cancer Cells

Kadhim

Mayah

Brooks

2020

Cancers

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Ionising radiation (IR) is commonly used for cancer therapy; however, its potential influence on the metastatic ability of surviving cancer cells exposed directly or indirectly to IR remains controversial. Metastasis is a multistep process by which the cancer cells dissociate from the initial site, invade, travel through the blood stream or lymphatic system, and colonise distant sites. This complex process has been reported to require cancer cells to undergo epithelial-mesenchymal transition (EMT) by which the cancer cells convert from an adhesive, epithelial to motile, mesenchymal form and is also associated with changes in glycosylation of cell surface proteins, which may be functionally involved in metastasis. In this paper, we give an overview of metastatic mechanisms and of the fundamentals of cancer-associated glycosylation changes. While not attempting a comprehensive review of this wide and fast moving field, we highlight some of the accumulating evidence from in vitro and in vivo models for increased metastatic potential in cancer cells that survive IR, focusing on angiogenesis, cancer cell motility, invasion, and EMT and glycosylation. We also explore the indirect effects in cells exposed to exosomes released from irradiated cells. The results of such studies need to be interpreted with caution and there remains limited evidence that radiotherapy enhances the metastatic capacity of cancers in a clinical setting and undoubtedly has a very positive clinical benefit. However, there is potential that this therapeutic benefit may ultimately be enhanced through a better understanding of the direct and indirect effects of IR on cancer cell behaviour.

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Section: The Effect Of Radiation On Cancer Cell Motility Invasion Amentioning

confidence: 98%

Section: The Effect Of Radiation On Angiogenesismentioning

confidence: 99%

Does Direct and Indirect Exposure to Ionising Radiation Influence the Metastatic Potential of Breast Cancer Cells

Kadhim

Mayah

Brooks

2020

Cancers

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“…These five subtypes have different abilities to metastasize to distant organs, specific pathways with the preferred metastatic sites, and different survival response after relapse [ 6 ]. Patients who have the luminal subtypes of breast cancer frequently for example have bone relapses; however, breast cancer of basal subtype often metastasizes to the lungs and brain, and cannot reach statistical significance in patients with liver relapse [ 2 , 4 ]. The biological subtypes of breast tumor can be defined by immunohistochemical (IHC) biomarkers or gene expression profiles [ 2 , 7 ].…”

Section: Introductionmentioning

confidence: 99%

“…The biological subtypes of breast tumor can be defined by immunohistochemical (IHC) biomarkers or gene expression profiles [ 2 , 7 ]. In general, the standard prognostic and predictive factors for breast cancer disease are human epidermal growth factor receptor 2 (HER2), progesterone receptor (PR), estrogen receptor (ER), and proliferation (Ki-67) status [ 4 , 8 ]. The choice of local or systemic treatment can vary related to these different subtypes of breast cancer [ 7 ].…”

Section: Introductionmentioning

confidence: 99%

Metastatic and triple-negative breast cancer: challenges and treatment options

Al-Mahmood

Sapiezynski

Garbuzenko

et al. 2018

Drug Deliv. and Transl. Res.

411

258

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The major current conventional types of metastatic breast cancer (MBC) treatments include surgery, radiation, hormonal therapy, chemotherapy, or immunotherapy. Introducing biological drugs, targeted treatment and gene therapy can potentially reduce the mortality and improve the quality of life in patients with MBC. However, combination of several types of treatment is usually recommended. Triple negative breast cancer (TNBC) accounts for 10–20% of all cases of breast carcinoma and is characterized by the low expression of progesterone receptor (PR), estrogen receptor (ER), and human epidermal growth factor receptor 2 (HER2). Consequently, convenient treatments used for MBC that target these receptors are not effective for TNBC which therefore requires special treatment approaches. This review discusses the occurrence of MBC, the prognosis and predictive biomarkers of MBC, and focuses on the novel advanced tactics for treatment of MBC and TNBC. Nanotechnology-based combinatorial approach for the suppression of EGFR by siRNA and gifitinib is described.

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“…Previous studies showed that cancer cells have higher CXCR4 expression levels compared to normal cells [25, 26]. In addition, over-expression of CXCR4 has been demonstrated to promote metastasis and associate with unfavorable prognosis in breast and lung cancer [27, 28]. Although CXCR4 has been reported to be relevant with various tumor progress and metastasis [29], the detailed molecular mechanisms of CXCR4 on osteosarcoma were still obscure.…”

Section: Introductionmentioning

confidence: 99%

Effect of CXCR4 on Apoptosis in Osteosarcoma Cells via the PI3K/Akt/NF-κβ Signaling Pathway

Jiang

et al. 2018

Cell Physiol Biochem

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Background/Aims: Osteosarcoma, the most common primary bone malignancy, arises from primitive transformed cells of mesenchymal origin with the worldwide increasing morbidity and mortality. Previous studies found apoptosis of osteosarcoma cells was essential for an effective manner to improve the progress of osteosarcoma, and CXCR4 has been demonstrated to be relevant with various tumor progress and metastasis. Methods: The proliferation of cells transfected with CXCR4 shRNA and control shRNA were measured by BrdU assay. Apoptosis was detected by flow cytometry. Apoptotic protein expression levels were detected by Western blot. Caspase activity was detected by Colorimetric Assay Kits using microplate reader. Activation of NF-κβ signaling after CXCR4 down-regulation in osteosarcoma cells was examined by constructing NF-κβ promoter luciferase reporter plasmid. The expression and activation of NF-κβ Signaling relevant protein were analyzed to investigate the relationship between Akt and NF-κβ signaling after the down-regulation of CXCR4 in osteosarcoma cells. Results: Down-regulation of CXCR4 significantly reduced the cell proliferation, while remarkably increased the cell apoptosis and apoptotic protein expression levels in osteosarcoma cells. Furthermore, down-regulation of CXCR4 induced cell apoptosis was caspase dependent in osteosarcoma cells. This study also showed CXCR4 down-regulation induced apoptosis through inhibiting PI3K/Akt/NF-κβ signaling pathway. In addition, endoplasmic reticulum stress (ERS) activation was involved in cell apoptosis induced down-regulation of CXCR4. Knockdown of partial ERS relevant proteins followed down-regulation of CXCR4 significantly inhibited cell apoptosis and the apoptotic protein expression levels. Conclusions: Taken together, the results demonstrated that down-regulation of CXCR4 could induce apoptosis of human osteosarcoma cells through inhibiting PI3K/Akt/NF-κβ signaling pathway, indicating that CXCR4 could be vital for the clinical therapy of osteosarcoma.

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Radiation-induced lung damage promotes breast cancer lung-metastasis through CXCR4 signaling

Cited by 43 publications

References 61 publications

Does Direct and Indirect Exposure to Ionising Radiation Influence the Metastatic Potential of Breast Cancer Cells

Does Direct and Indirect Exposure to Ionising Radiation Influence the Metastatic Potential of Breast Cancer Cells

Metastatic and triple-negative breast cancer: challenges and treatment options

Effect of CXCR4 on Apoptosis in Osteosarcoma Cells via the PI3K/Akt/NF-κβ Signaling Pathway

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