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

ABSTRACT: When co-cultured, HER2 L755S mutant cells are induced to proliferate when coming into close contact with PIK3CA E545K mutant cells We used a microarray to compare transciptome-wide expression levels between HER2 L755S cells, PIK3CA E545K cells, and co-cultures containing both cell types.

ORGANISM(S): Homo sapiens

PROVIDER: GSE165065 | GEO | 2021/03/18

REPOSITORIES: GEO

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

Project description: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.

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

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PIK3CA-dependent hepatocarcinogenesis. A microarray comparing PIK3CA E545K and H1047R injected mice compared to age matched controls.

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Expression data PIK3CA E545K vs PIK3CA H1047R stably transfected in human HCC cell lines

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Project description:The purpose of this research is to study the mechanism of the synergistic effect combining EZH2 inhibition and PI3K inhibition. In this study, we observed that the PIK3CA-mutant or amplified lung cancer cells were more sensitive to EZH2 inhibition. PIK3CA E545K, the most common mutation in lung cancer, harbored a modest transformation capacity along with p53 loss in lung epithelial cells, and developed adenocarcinoma autochthonously. EZH2 inhibitor synergized with PI3K inhibitor in human cancer cells in vitro and worked together efficiently in vivo. Mechanistically, EZH2 inhibition cooperated with PI3K inhibition to produce a more potent suppression of phospho-AKT downstream of PI3K.

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Mutant PI3K cooperates with HER2 to promote mammary tumor formation and induces trastuzumab resistance in vivo

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Activating Mutations in PIK3CA result in Widespread Modulation of the Tyrosine Phosphoproteome

Project description:The human oncogene PIK3CA is frequently mutated in human cancers. The two hotspot mutations in PIK3CA, E545K and H1047R, have been shown to regulate widespread signaling events downstream of AKT. However, the impact of these activating mutations on the tyrosine phosphorylation signaling in the cell has not been studied. Here, we performed a global phosphotyrosine profiling using isogenic knockin cell lines containing these activating mutations. We identified 824 unique phosphopeptides from 308 proteins. We found a surprisingly widespread modulation of tyrosine phosphorylation levels of proteins in the knockin mutant cells, with many of the regulated proteins involved in important biological processes, including those in the cytoskeletal migration pathways and kinase regulated signaling. We observed a widespread modulation of the tyrosine kinome, with 24 of the tyrosine kinases showing either upregulation or downregulation in phosphorylation levels. Many of the regulated phosphosites that we identified were located in the kinase domain or the canonical activating sites, indicating that the kinases were active and hence their downstream signaling pathways. Our study thus shows that the activating mutations in PIK3CA result in widespread tyrosine signaling regulation, in addition to the serine/threonine signaling pathways activated by the canonical PI3K-AKT axis.

2018-10-24 | PXD001460 | Pride

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