Transcriptomics

Dataset Information

35

Endogenous expression of an oncogenic PI3K mutation leads to activated PI3K pathway signaling and an invasive phenotype


ABSTRACT: The PTEN/PI3K pathway is commonly mutated in cancer and therefore represents a rational target for therapeutic intervention. In order to investigate the primary phenotype(s) mediated by mutant PIK3CA in a clean and highly patient-relevant context, we utilized a non-tumorigenic MCF10A parental and isogenic knock-in cell line that harbors a common activating PIK3CA kinase domain mutation (H1047R). We found that introduction of an endogenously mutated PIK3CA primarily results in a marked epithelial-mesenchymal transition (EMT) and invasive phenotype compared to isogenic wild-type cells. Moreover, a potent and selective inhibitor of PIK3CA (GDC-0941) was highly effective and selective on reversing this phenotype compared to cell-proliferation, highlighting a potential new paradigm for studying PI3K-pathway targeted agents. Keywords: Expression Array Overall design: Gene expression profiles from a parental MCF10A breast line and an MCF10A clone that has a PI3K activating mutation (H1047R) knocked-in. We plated the cells in 10cm dishes overnight in media with serum, but lacking EGF or insulin. DMSO or GDC-0941 (PI3K inhibitor) at an EC50 concentration were added to triplicate plates of cells in the morning. After 4 hours the RNA was harvested using the Qiagen RNeasy kit. There are 12 samples total.

INSTRUMENT(S): [HG-U133_Plus_2] Affymetrix Human Genome U133 Plus 2.0 Array

ORGANISM(S): Homo sapiens  

SUBMITTER: Peter Haverty  

PROVIDER: GSE17785 | GEO | 2011-08-10

SECONDARY ACCESSION(S): PRJNA117883

REPOSITORIES: GEO

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