About NCI-H1734
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.
NCI-H1734 Tumor Kinetics in the SRG™ Rat
![H-1734-graph](https://www.herabiolabs.com/storage/2023/07/H-1734-graph.jpg)
In vivo, NCI-H1734 cells produce firm, vascularized tumors that tend to exhibit slow growth. This tumor phenotype in vivo reflects the characteristics of NCI-H1734 cells and provides a platform for studying tumor growth dynamics, angiogenesis, and therapeutic responses in a more complex physiological context.
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References (MLA):
- Addeo, Alfredo, et al. “Kras G12C Mutations in NSCLC: From Target to Resistance.” MDPI, 21 May 2021, www.mdpi.com/2072-6694/13/11/2541.
- Fong, Jason T., et al. “Alternative Signaling Pathways as Potential Therapeutic Targets for Overcoming EGFR and C-MET Inhibitor Resistance in Non-Small Cell Lung Cancer.” PLOS ONE, 4 Nov. 2013, journals.plos.org/plosone/article?id=10.1371%2Fjournal.pone.0078398.
- Hong, Weiwei, et al. “Prognostic Value of EGFR 19‑del and 21‑L858R Mutations in Patients with Non‑small Cell Lung Cancer.” Oncology Letters, 1 Aug. 2019, www.spandidos-publications.com/10.3892/ol.2019.10715.
- Latour, Sylvain, and Claire Aguilar. “XIAP Deficiency Syndrome in Humans.” Seminars in Cell & Developmental Biology, 7 Feb. 2015, www.sciencedirect.com/science/article/abs/pii/S1084952115000270?via%3Dihub.