Molecular Playground/IntegrinBeta1: Difference between revisions
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'''Banner:''' Cancer cell migration, Integrin Beta 1 binds to ECM proteins and allows for 3D ''in vitro'' cell migration | '''Banner:''' Cancer cell migration, Integrin Beta 1 binds to ECM proteins and allows for 3D ''in vitro'' cell migration | ||
<Structure load='3VI4' size='350' frame='true' align='right' caption='Integrin Beta 1 | <Structure load='3VI4' size='350' frame='true' align='right' caption='Integrin Beta 1 Alpha 5' scene='60/609772/Integrinb1alpha5/1' /> | ||
==Structure== | ==Structure== | ||
Blue-Alpha 5 chain | Blue-Alpha 5 chain | ||
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==Integrins and cancer== | ==Integrins and cancer== | ||
Integrins binding to the extracellular matrix provide cells the ability to migrate and remodel the surrounding microenvironment. For these reasons, integrins are extremely important in cancer metastasis, and the progression of solid tumors. Cells bind to extracellular matrix proteins, like<scene name='60/609772/Rgd_bound/2'>RGD (black) on fibronectin</scene>, with integrins to stimulate survival, migration/invasion, and proliferation [2]. High expression of integrin beta 1 has been shown to drive primary tumor progression and metastasis, but targeting integrins for cancer treatment has seen limited success [3]. Likely, these failures stem from differential integrin expression between cancer cells, and new technologies to screen cancer cell populations are being developed to screen for affective therapies [4]. These technologies will likely allow for more selective treatment and better clinical efficacy for integrin inhibitors. | Integrins binding to the extracellular matrix provide cells the ability to migrate and remodel the surrounding microenvironment. For these reasons, integrins are extremely important in cancer metastasis, and the progression of solid tumors. Cells bind to extracellular matrix proteins, like<scene name='60/609772/Rgd_bound/2'> peptide RGD (black) on fibronectin</scene>, with integrins to stimulate survival, migration/invasion, and proliferation [2]. High expression of integrin beta 1 has been shown to drive primary tumor progression and metastasis, but targeting integrins for cancer treatment has seen limited success [3]. Likely, these failures stem from differential integrin expression between cancer cells, and new technologies to screen cancer cell populations are being developed to screen for affective therapies [4]. These technologies will likely allow for more selective treatment and better clinical efficacy for integrin inhibitors. | ||
==Studying Integrin Beta-1'' in vitro''== | ==Studying Integrin Beta-1'' in vitro''== | ||