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Gene expression analysis of single and co-cultured HER2 L755S mutants in MCF-10A background

ABSTRACT: PIK3CA E545K mutants induce epidermal growth-factor independent proliferation of HER2 L755S mutants through a contact-mediated mechanism. We used RT2 Profiler PCR Arrays to study changes in gene expression in the HER2 L755S mutants when co-cultured with the PIK3CA E545K mutants and compared it to the HER2 L755S mutants grown in isolation.

ORGANISM(S): Homo sapiens

PROVIDER: GSE165150 | GEO | 2021/03/18

REPOSITORIES: GEO

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Expression data from HER2 L755S, PIK3CA E545K, and co-cultured cells in the MCF-10A background

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Project description:HER2 (ERBB2) gene amplification and PIK3CA mutations often co-occur in breast cancer, and aberrant activation of the PI3K pathway has been implicated in resistance to HER2-directed therapies. We have created a mouse model of HER2-overexpressing (HER2+), PIK3CAH1047R-mutant breast cancer. Mice expressing both human HER2 and mutant PIK3CA in their mammary glands developed tumors with a significantly shorter latency compared to mice expressing either oncogene alone. By microarray analysis, HER2-driven tumors clustered with the luminal subtype, whereas HER2+PIK3CA and PIK3CA-driven tumors were associated with the claudin-low breast cancer subtype. In accordance, PIK3CA and HER2+PIK3CA tumors expressed elevated levels of EMT and stem cell markers, and cells from HER2+PIK3CA tumors more efficiently formed mammospheres, providing further evidence that activated PIK3CA may enrich for cancer stem cells. Finally, HER2+PIK3CA tumors are resistant to the HER2 antibody trastuzumab; resistance is partially reversed by the addition of a PI3K inhibitor. Taken together, these studies suggest that the co-expression of HER2 and PI3KH1047R in the mouse mammary gland accelerates the formation of aggressive, trastuzumab-resistant tumors. referenceXsample

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