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We performed gene expression profiles of human bronchoalveolar epithelial cells (HBEC) transduced with GFP labeled murine focal adhesion kinase (PMX-Purom-GFP-mFAK) or GFP control empty vector counterpart (PMX-Purom-GFP-empty)

ABSTRACT: The goal if this project was to determine the cellular pathways affected by FAK protein overexpression downstream of oncogenic KRAS and RHOA in normal lung epithelium. In addition, we aim to characterize the potential downstream modulators of cell growth and migration upon FAK hyperactivation. We identified pathways in DNA damage, cell growth, apoptosis and cytoskeleton remodeling pertaining to tissue differentiation and carcinogenesis signature respectively. For this study, two duplicate samples were analyzed in triplicate arrays for a total of 6 data poinst per condition. The groups compared were PMX-Purom-GFP-mFAK against PMX-Purom-GFP-emty.

ORGANISM(S): Homo sapiens

SUBMITTER: Jerfiz Constanzo

PROVIDER: E-GEOD-72470 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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We performed gene expression profiles of human bronchoalveolar epithelial cells (HBEC) transduced with GFP labeled murine focal adhesion kinase (PMX-Purom-GFP-mFAK) or GFP control empty vector counterpart (PMX-Purom-GFP-empty)

Project description:The goal if this project was to determine the cellular pathways affected by FAK protein overexpression downstream of oncogenic KRAS and RHOA in normal lung epithelium. In addition, we aim to characterize the potential downstream modulators of cell growth and migration upon FAK hyperactivation. We identified pathways in DNA damage, cell growth, apoptosis and cytoskeleton remodeling pertaining to tissue differentiation and carcinogenesis signature respectively.

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Gene expression profiles of human bronchoalveolar epithelial cells (HBEC) transduced with GFP labeled murine focal adhesion kinase (PMX-Purom-GFP-mFAK) or in combination with SUMO ligase Pias1

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