Expression data from MM231 and MM231-FGD5-cas9 breast cancer cells
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PROVIDER: PRJNA603236 | ENA |
REPOSITORIES: ENA
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Project description:To identify the differiational genes and pathways in MM231 and MM231-FGD5-cas9, we examined the microarray gene expression profile of MM231 breast cancer cells vs FGD5-cas9 cells. Ectopic expression or activation of EGFR is found in most TNBCs, and EGFR inhibitors can suppress TNBC growth in vitro. However, these agents exhibit limited efficacy in TNBC patients, possibly due to the nonkinase oncogenic functions of EGFR and the compensatory effects of other oncogenic activities following anti-EGFR therapy. Here, we identified a positive correlation between EGFR and FGD5 expression in TNBC samples. FGD5 deletion attenuated TNBC initiation and progression by decreasing EGFR stability and expression. Moreover, the proteins involved in mutual compensation of EGFR signaling were significantly downregulated in FGD5-deleted TNBC cells. Mechanistically, FGD5 interacted with EGFR to maintain EGFR stability by impeding EGFR ubiquitylation and degradation mediated by the E3 ligase ITCH; disrupting the FGD5-EGFR interaction accelerated EGFR degradation and produced robust anti-TNBC activity. Our study shows that targeted degradation of EGFR through disrupting the FGD5-EGFR interaction is a promising therapeutic strategy for the TNBC subtype of breast cancer.
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Project description:Purpose: According to the previous analysis results of gene regulation in fetal heart tissues with tetralogy of Fallot (ToF), we constructed the ceRNA mediated network driven by lncRNAs using a causal inference framework based on the expression correlations and validated miRNA-lncRNA/mRNA evidences. Totally 4 lncRNAs were identified as hub lncRNAs in the network, and FGD5-AS1 was focused for further loss-of-function investigation. Methods: The specific shRNAs against FGD5-AS1 (sh-FGD5-AS1) as well as the corresponding negative control (sh-NC) were constructed along with lentiviral vector respectively. Then the CCC-HEH-2 human cardiac myocytes cell lines were infected with lentivirus and followed puromycin treatment for several days. The knockdown efficiencies of the FGD5-AS1 expression were validated by qPCR. The landscape of accessible chromatin in control and knockdown CCC-HEH-2 cell lines were observed using ATAC-Seq. Conclusions: Our data reveal a unique different chromatin state between wild type and FGD5-AS1 knockdown CCC-HEH-2 cells.
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