Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA248819 | ENA |
REPOSITORIES: ENA
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Project description:Advanced head and neck squamous cell carcinomas (HNSCC) are frequently drug resistant and have a mortality rate of 40%. We have previously shown that E2F7 may contribute to drug sensitivity. In the present study, we conducted an M-bM-^@M-^Somics screen to identify factors that were responsible for E2F7-dependent resistance to anthracyclines by HNSCC. We provide, in vitro, in vivo and patient data that identifies the existence of a novel E2F7/Sphingosine kinase 1/Sphingosine-1-phosphate/AKT axis that regulates sensitivity to anthracyclines in HNSCC. Specifically, we show that E2F7-dependent sensitivity to doxorubicin occurs via induction of the sphingosine kinase 1/AKT axis. We also show that pharmacological inhibition of Sphingosine kinase 1 or AKT sensitizes SCC cells to the cytotoxic actions of doxorubicin in vitro and in vivo. Combined, these findings highlight a novel mechanism through which SCC cells acquire resistance to anthracyclines and identify specific pharmacological combinations that could be used to treat SCC. Duplicate total RNA isolated from i) untreated, KJD cells, ii) 1M-BM-5M doxorubicin-treated KJD cells, iii) control plasmid (pcDNA3) transfected, untreated KJD cells, iv) control plasmid (pcDNA3) transfected, 1M-BM-5M doxorubicin-treated KJD cells, v) E2F7 expression plasmid transfected, untreated KJD cells, vi) E2F7 expression plasmid transfected, 1M-BM-5M doxorubicin-treated KJD cells, vii) untreated, SCC25 cells, viii) 1M-BM-5M doxorubicin-treated SCC25 cells, ix) control siRNA (GFPsiRNA) transfected, untreated SCC25 cells, x) control siRNA (GFPsiRNA) transfected, 1M-BM-5M doxorubicin-treated SCC25 cells, xi) E2F7siRNA transfected, untreated SCC25 cells, xii) E2F7siRNA transfected, 1M-BM-5M doxorubicin-treated SCC25 cells were hybridised to an RNA microarray to identify genes which are downstream of E2F7 and regulate chemosensitivity in SCC.
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Project description:Advanced head and neck squamous cell carcinomas (HNSCC) are frequently drug resistant and have a mortality rate of 40%. We have previously shown that E2F7 may contribute to drug sensitivity. In the present study, we conducted an –omics screen to identify factors that were responsible for E2F7-dependent resistance to anthracyclines by HNSCC. We provide, in vitro, in vivo and patient data that identifies the existence of a novel E2F7/Sphingosine kinase 1/Sphingosine-1-phosphate/AKT axis that regulates sensitivity to anthracyclines in HNSCC. Specifically, we show that E2F7-dependent sensitivity to doxorubicin occurs via induction of the sphingosine kinase 1/AKT axis. We also show that pharmacological inhibition of Sphingosine kinase 1 or AKT sensitizes SCC cells to the cytotoxic actions of doxorubicin in vitro and in vivo. Combined, these findings highlight a novel mechanism through which SCC cells acquire resistance to anthracyclines and identify specific pharmacological combinations that could be used to treat SCC.
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Project description:This SuperSeries is composed of the following subset Series: GSE14859: ArrayCGH mapping of chromosome 3 aberrations in lung Squamous Cell Carcinoma (SCC) GSE14883: SOX2 overexpression effect on human lung squamous cells GSE15079: ArrayCGH mapping of the recurrent 3q26.3-q27mplifications in lung Squamous Cell Carcinoma (SCC) Refer to individual Series
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