Toward an Integrative Analysis of the Tumor Microenvironment in Ovarian Epithelial Carcinoma

Serio, Ryan N

doi:10.1007/s12307-011-0092-5

Cited by 2 publications

(3 citation statements)

References 126 publications

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“…(PI3K) and AKT (Velling et al, 2004), FAK (Wennerberg et al, 2000), as well as Src (Meng and Lowell, 1998). b1 integrin has also been shown to modulate expression of E-cadherin (Serio, 2012) and the integrins a6 and b4 (Huck et al, 2010). Alterations to these pathways might affect both invadopodia formation and cell invasion.…”

Section: Discussionmentioning

confidence: 99%

SNARE-dependent interaction of Src, EGFR and β1 integrin regulates invadopodia formation and tumor cell invasion

Williams

Coppolino

2014

Journal of Cell Science

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Acquisition of an invasive phenotype is prerequisite for tumor metastasis. Degradation of the extracellular matrix (ECM), and subsequent invasion by tumor cells, is mediated, in part, through subcellular structures called invadopodia. Src-dependent cytoskeletal rearrangements are required to form invadopodia, and here we identify an association between Src, epidermal growth factor receptor (EGFR), and b1 integrin that facilitates invadopodia formation. The association of Src, EGFR and b1 integrin is dependent upon membrane traffic that is mediated by syntaxin13 (officially known as STX12) and SNAP23; a similar dependence on these two SNARE proteins was observed for invadopodium-based matrix degradation and cell invasion. Inhibition of SNARE function impaired the delivery of Src and EGFR to developing invadopodia, as well as the b1-integrin-dependent activation of Src and phosphorylation of EGFR on Tyr residue 845. We also identified an association between SNAP23 and b1 integrin, and inhibition of b1 integrin increased this association, whereas the interaction between syntaxin13 and SNAP23 was reduced. The results suggest that SNARE-dependent trafficking is regulated, in part, by b1 integrin and is required for the delivery of Src and EGFR to sites of invadopodia formation in order to support tumor cell invasion.

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Section: Discussionmentioning

confidence: 99%

SNARE-dependent interaction of Src, EGFR and β1 integrin regulates invadopodia formation and tumor cell invasion

Williams

Coppolino

2014

Journal of Cell Science

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“…The tumor microenvironment can facilitate the EMT program in HSGC [27]. Proteins and enzymes derived from the tumor, including cytokines (TGFb, TNFa, IGF, and PDGF), transcriptional factors (Snail and Slug, Twist and FOXC2), and metalloproteinases (increased bcatenin in cytoplasm) can activate EMT in cancer cells.…”

Section: Gene-expression Of Embryonic Stem Cells [Escs]mentioning

confidence: 99%

“…The spread of disease to the peritoneum is an early event that is favored by the tumor microenvironment in the coelomic epithelium. Current evidence suggests a major role for EMT in the dissemination of EOC to the peritoneum and in the genesis of OC [27].…”

Section: Carcinogenesis Model In Peritoneal Carcinomatosismentioning

confidence: 99%

Peritoneal carcinomatosis: A malignant disease with an embryological origin?

et al. 2015

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Toward an Integrative Analysis of the Tumor Microenvironment in Ovarian Epithelial Carcinoma

Abstract: Ovarian epithelial carcinomas are heterogeneous malignancies exhibiting great diversity in histological phenotypes as well as genetic and epigenetic aberrations.

Cited by 2 publications

References 126 publications

SNARE-dependent interaction of Src, EGFR and β1 integrin regulates invadopodia formation and tumor cell invasion

SNARE-dependent interaction of Src, EGFR and β1 integrin regulates invadopodia formation and tumor cell invasion

Peritoneal carcinomatosis: A malignant disease with an embryological origin?

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