Derivation
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This isogenic cell line was created at ATCC by using CRISPR gene editing technology.
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Antigen Expression
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The cells are positive for keratin by immunoperoxidase staining.
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Comments
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The anaplastic lymphoma kinase (ALK) genetic abnormality is a key oncogenic driver, especially in non-small cell lung cancer. The EML4-ALK gene fusion caused by a chromosomal inversion can produce constitutively active ALK tyrosine kinase protein, which leads to enhanced cell survival and cell proliferation. There are multiple EML4-ALK fusion variants, with the most prevalent being variant 1 (E13; A20) in which EML4 intron 13 is fused with ALK intron 20. ATCC isogenic cell line CCL-185IG was created at ATCC by using CRISPR gene editing technology, and contains EML4-ALK fusion variant 1 (E13; A20). This isogenic cell line (CCL-185IG) was created from the A549 parental cell line, CCL-185, a non-small cell lung cancer cell line. The EML4-ALK fusion in CCL-185IG has been intensively validated at the genomic, transcript and protein levels. Furthermore, CCL-1851G is more sensitive to the ALK inhibitor crizotinib when compared to its parental cell line. CCL-185IG can be a useful model to study tyrosine kinase signaling pathway, and to screen ALK inhibitors in anti-cancer drug discovery and development.
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