NCI-H1734 Cell Line

The NCI-H1734 cell line is derived from human epithelial non-small-cell lung carcinoma and was obtained from the lung tissue of a 56-year-old female patient. It was established in September 1987 and has since played a crucial role in advancing our understanding of lung cancer biology. NCI-H1734 cells are cultured optimally in RPMI medium 1640 supplemented with 10% fetal bovine serum (FBS).

This cell line exhibits several important genetic alterations that contribute to its oncogenic phenotype and therapeutic responsiveness. NCI-H1734 cells feature the L858R mutation in exon 21 of the epidermal growth factor receptor (EGFR). This mutation results in a single amino acid substitution in the EGFR protein, leading to its constitutive activation. The EGFR pathway plays a crucial role in cell growth, survival, and proliferation, and its dysregulation is frequently observed in non-small-cell lung carcinoma. The presence of the L858R mutation in NCI-H1734 cells makes this cell line a valuable model for studying the role of EGFR in lung cancer oncogenesis and investigating therapeutic strategies targeting EGFR signaling.

In addition, NCI-H1734 cells harbor a KRAS G12C mutation. KRAS is a member of the RAS family of oncogenes and plays a central role in cell signaling networks that regulate proliferation, survival, and differentiation. The specific G12C mutation in KRAS observed in NCI-H1734 cells results in constitutive activation of downstream signaling pathways, contributing to cellular transformation and tumor progression. The presence of both EGFR and KRAS mutations in NCI-H1734 cells underscores the complexity and heterogeneity of non-small-cell lung carcinoma and provides an excellent model for studying the interplay between these key oncogenic drivers.

Furthermore, NCI-H1734 cells exhibit overexpression of tyrosine-protein kinase Met (c-Met). c-Met is a receptor tyrosine kinase involved in various cellular processes, including cell growth, survival, motility, and invasion. Overexpression of c-Met in NCI-H1734 cells indicates its potential contribution to the malignant phenotype of this cell line and its involvement in promoting lung cancer progression. Drug sensitivity studies have revealed that NCI-H1734 cells are primarily sensitive to DNA alkylating agents, which cause structural damage to DNA.

NCI-H1734 cells have shown sensitivity to XIAP (X-linked inhibitor of apoptosis protein) targeted agents. XIAP is an anti-apoptotic protein that confers resistance to cell death pathways, and targeting XIAP has emerged as a potential therapeutic strategy for enhancing the efficacy of anticancer treatments. Conversely, NCI-H1734 cells have exhibited resistance to cediranib, a tyrosine kinase inhibitor targeting vascular endothelial growth factor (VEGF) receptors involved in angiogenesis.

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