Depletion of beta1 integrins in triple negative breast cancer cells causes extensive alterations in gene expression profiles

ABSTRACT: Interactions with the extracellular matrix (ECM) through integrin adhesion receptors provide cancer cells with physical and chemical cues that act in concert with growth factors to support survival and proliferation. Preclinical studies testing beta1 integrin antagonists in (breast) cancer models have shown inhibition of tumor growth and sensitization to radio- or chemotherapy and these strategies are currently evaluated in clinical trials. Here, we show that disruption of beta1 integrin-mediated ECM adhesion attenuates breast tumor growth but dissemination to the lungs from such small tumors can be markedly enhanced. beta1 integrin downregulation induces compensatory upregulation of beta3 integrins, but increased beta3 expression does not lead to enhanced lung metastasis. Instead, b

ORGANISM(S): Mus musculus

SUBMITTER: John Meerman 

PROVIDER: E-MTAB-2185 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress