The Role of α2β1 and α3β1 Integrin Receptors in the Initial Anchoring of MDA-MB-231 Human Breast Cancer Cells to Cortical Bone Matrix

Lundström, Åse; Holmbom, Johanna; Lindqvist, Christer; Nordström, Tommy

doi:10.1006/bbrc.1998.9389

Cited by 49 publications

(44 citation statements)

References 16 publications

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“…Previous studies have demonstrated that MDA-MB-231 cells attach equally well on several ECM proteins, such as type I collagen, ®bronectin, laminin-1 and vitronectin (Lichtner et al, 1998;Lundstrom et al, 1998;van der Pluijm et al, 1997;Wong et al, 1998), and we found the same here. Also of note, no di erences in cell survival were observed when MDA-MB-231 cells were plated on di erent matrix substrates or on the non-integrin ligand polylysine for extended periods of time in the absence of any drug treatment (not shown).…”

Section: Resultssupporting

confidence: 87%

“…The survival e ect of collagen I was speci®cally and signi®cantly inhibited by antibodies against the a2b1 integrin, but not the a1b1 or the a3b1 integrins ( Figure 1c). Cell attachment assays demonstrated that a2b1 integrin, which is a known collagen receptor, mediates MDA-MB-231 cell attachment to collagen I (data not shown) (Lichtner et al, 1998;Lundstrom et al, 1998;van der Pluijm et al, 1997). Taken together, our results indicate that signaling via the a2b1 and a5b1 integrins signi®cantly inhibits chemotherapeutic agent-induced apoptosis in MDA-MB-231 cells.…”

Section: Resultsmentioning

confidence: 93%

“…Thus, MDA-MB-231 cells are known to metastasize avidly to bone, in which type I collagen is very abundant (Coleman and Rubens, 1987). Further, it has been shown that a2b1 integrin-mediated attachment to collagen I is necessary for bone metastasis to take place by breast cancer cells (Lundstrom et al, 1998;van der Pluijm et al, 1997). In turn, laminin-a6b1 integrin interaction has been shown to enhance survival and in vivo tumor growth of MDA-MB-435 cells (Wewer et al, 1997).…”

Section: Discussionmentioning

confidence: 99%

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Integrin signaling inhibits paclitaxel-induced apoptosis in breast cancer cells

2001

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Inherent or acquired drug resistance is one of the major problems in chemotherapy. The mechanisms by which cancer cells survive and escape the cytotoxic e ects of chemotherapeutic agents are essentially unknown. In the present study, we demonstrate that in the MDA-MB-231 and MDA-MB-435 breast cancer cells, ligation of b1 integrins by their extracellular matrix ligands inhibits signi®cantly apoptosis induced by paclitaxel and vincristine, two microtubule-directed chemotherapeutic agents that are widely used in the therapy of breast cancer. We show that b1 integrin signaling inhibits drug-induced apoptosis by inhibiting the release of cytochrome c from the mitochondria in response to drug treatment. Further, integrin-mediated protection from drug-induced apoptosis and inhibition of cytochrome c release are dependent on the activation of the PI 3-kinase/Akt pathway. Our results identify b1 integrin signaling as an important survival pathway in drug-induced apoptosis in breast cancer cells and suggest that activation of this pathway may contribute to the generation of drug resistance. Oncogene (2001) 20, 4995 ± 5004.

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Section: Resultssupporting

confidence: 87%

Section: Resultsmentioning

confidence: 93%

Section: Discussionmentioning

confidence: 99%

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Integrin signaling inhibits paclitaxel-induced apoptosis in breast cancer cells

2001

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“…Indeed, other groups have shown that in prostate cancer, elevated levels of RhoC enhance collagen I-␣ 2 ␤ 1 signaling and promote tumor metastasis to the bone matrix, which contains abundant levels of collagen type I (30,31). In addition, the attachment of MDA-MB-231 cells to cortical bone disks was blocked by as much as 75% when cells were pretreated with monoclonal antibodies to ␣ 2 and ␤ 1 subunits of the integrin family (32).…”

Section: Discussionmentioning

confidence: 99%

Integrin α2β1 Mediates Tyrosine Phosphorylation of Vascular Endothelial Cadherin Induced by Invasive Breast Cancer Cells

Haidari

Zhang

Caivano

et al. 2012

Journal of Biological Chemistry

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Background:The disruption of endothelial barrier function by tumor cells was studied. Results: The attachment of tumor cells to endothelial cells leads to the disorganization of endothelial adherens junction. Conclusion: Interaction of tumor cells with endothelial cells alters endothelial signaling and facilitates cancer cell diapedesis. Significance: This study introduces new therapeutic targets for treating metastatic breast cancer.

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“…Integrin α2 is a collagen receptor that is mainly expressed on platelets and epithelial cells [27]. Integrin α2β1 was found to facilitate integrin-mediated attachment to collagen type I during the metastasis of breast cancer cells to bone [28]. The binding of collagen I to α2β1 integrin was also shown to promote the malignant phenotype of pancreatic ductal adenocarcinoma [29].…”

Section: Introductionmentioning

confidence: 99%

Association of hOGG1 Ser326Cys, ITGA2 C807T and TNF-A -308G>A Polymorphisms with the Risk of NPC

Eng-Zhuan¹,

Munn-Sann²,

Pp³

et al. 2017

J Mol Genet Med

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Background: Nasopharyngeal carcinoma (NPC) is a rare form of cancer. NPC is the 4th most common cancer in Malaysia and the incidence rate for Malaysian Chinese is exceptionally high compared to other races. NPC is considered as a relatively radiosensitive tumor and patients diagnosed at early stages tend to survive longer compared to those who with advanced disease. Given that early symptoms of NPC are non-specific, and that the nasopharynx is relatively inaccessible, less invasive screening methods such as biomarker screening might be the key to improve NPC survival and management.Methodology: A matched case-control study was conducted to investigate the effect of hOGG1 Ser326Cys, ITGA2 C807T and TNF-α -308G>A polymorphisms on the risk of nasopharyngeal carcinoma and all-cause survival. hOGG1 gene encodes for a DNA glycosylase, a protein that is involved in DNA repair. ITGA2 is the alpha subunit of the transmembrane receptor integrin and is mainly responsible for cell-cell and cell-extracellular matrix interaction. TNF-α is a cytokine that is released by immune cells during inflammation. Restriction fragment length polymorphism-polymerase chain reaction (RFLP-PCR) was used to process DNA genotyping studies involving all aforementioned gene polymorphisms. Conditional logistic regression was used for the analysis of NPC risk on gene polymorphisms, controlling for cigarette smoking, salted fish and alcohol consumption.Results: Conditional logistic regression showed that NPC cases were more likely to ever consume salted fish during childhood compared to controls (OR=1.80, 95% CI=1.32-2.46, p<0.01). Individuals with previous smoking history were also at higher risk of NPC (OR=1.96, 95% CI=1.37-2.81, p<0.01). No significant difference was found between NPC cases and controls for alcohol consumption. No significant association was observed between hOGG1 Ser326Cys, ITGA2 C807T, TNF-α -308G>A polymorphisms with NPC risk. Conclusion:None of the aforementioned polymorphisms showed significant association in increasing NPC risk individually.

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The Role of α2β1 and α3β1 Integrin Receptors in the Initial Anchoring of MDA-MB-231 Human Breast Cancer Cells to Cortical Bone Matrix

Cited by 49 publications

References 16 publications

Integrin signaling inhibits paclitaxel-induced apoptosis in breast cancer cells

Integrin signaling inhibits paclitaxel-induced apoptosis in breast cancer cells

Integrin α2β1 Mediates Tyrosine Phosphorylation of Vascular Endothelial Cadherin Induced by Invasive Breast Cancer Cells

Association of hOGG1 Ser326Cys, ITGA2 C807T and TNF-A -308G>A Polymorphisms with the Risk of NPC

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