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Expression data from EML4-ALK overexpression in HEK293 cell line and EML4-ALK knockdown in H2228 lung cancer cell line.

ABSTRACT: Expression data from EML4-ALK overexpression in HEK293 cell line and EML4-ALK knockdown in H2228 lung cancer cell line.

PROVIDER: PRJNA731500 | ENA |

REPOSITORIES: ENA

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Expression data from EML4-ALK overexpression in HEK293 cell line and EML4-ALK knockdown in H2228 lung cancer cell line.

Project description:We demonstrate that EML4-ALK siRNAs significantly reduced cell viability in EML4-ALK postive lung cancer cell lines,while overexpression of EML4-ALK increased cell viability in HEK293 cells in vitro. The aim of this study was to analyze the EML4-ALK regulated gene expression in lung cancer.

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Alectinib-resistant NSCLC harboring EML4-ALK cells: Parental vs. Alectinib-resistant

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Alectinib-resistant NSCLC harboring EML4-ALK cells: Parental vs. Alectinib-resistant

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EML4-ALK variant-specific genetic interactions shape lung tumorigenesis

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EML4-ALK variant-specific genetic interactions shape lung tumorigenesis

Project description:Oncogenic fusions of EML4 and ALK occur in ~5% of lung adenocarcinomas. EML4- ALK variants have distinct breakpoints within EML4, but the functional differences among these variants remain poorly understood. Here we use CRISPR/Cas9 somatic genome editing to generate autochthonous mouse models of the two most common EML4-ALK variants and show that V3 is more oncogenic than V1. By employing multiplexed genome editing and quantifying the effects of 29 putative tumor suppressor genes on V1- and V3-driven lung cancer growth in vivo we show that many tumor suppressor genes have dramatically variant-specific effects on tumorigenesis. Pharmacogenomic analyses suggest that tumor genotype can also modify responses to therapy. Analysis of a large human EML4-ALK lung cancer cohort identified differences in the genomic landscape depending on the EML4-ALK variant. These findings demonstrate functional heterogeneity between EML4-ALK variants, suggesting that EML4-ALK variants behave more like distinct oncogenes than a uniform entity. More broadly, these findings highlight the dramatic impact of oncogenic fusions partner proteins and coincident tumor suppressor gene alterations on the biology of oncogenic fusion driven cancer.

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Expression data from IL4 treatment in EML4-ALK-positive lung cancer cells.

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