The Nras Knockout LLC Cell Line is a CRISPR/Cas9-edited knockout cell line derived from the mouse Lewis lung carcinoma (LLC) line. This product features targeted disruption of the Nras gene, eliminating functional NRAS protein expression and providing a defined loss-of-function model. The knockout was generated using CRISPR/Cas9-mediated gene editing, resulting in a stable cell line suitable for a wide range of in vitro and in vivo applications in cancer signaling research. The engineered cells retain the parental LLC background while lacking NRAS-driven signal transduction, enabling precise dissection of RAS pathway functions.
LLC cells originate from a C57BL/6 mouse Lewis lung carcinoma and are a widely used syngeneic model for lung cancer research. These cells display aggressive tumorigenic properties, including rapid proliferation, migration, and the capacity to form tumors in immunocompetent mice. The LLC line is particularly valuable for studying tumor-host interactions, metastasis, and immune evasion mechanisms. As a well-characterized murine lung cancer cell line, LLC provides a robust platform for investigating oncogenic signaling and evaluating therapeutic interventions in a physiologically relevant context.
NRAS is a small GTPase that functions as a molecular switch in signal transduction, cycling between an active GTP-bound state and an inactive GDP-bound state. It is activated downstream of receptor tyrosine kinases such as EGFR and FGFR, through adaptor proteins GRB2 and the guanine nucleotide exchange factor SOS. Active NRAS promotes signaling via the MAPK/ERK cascade by recruiting and activating RAF kinases, which then phosphorylate MEK1/2 and ERK1/2, and concurrently stimulates the PI3K/AKT/mTOR pathway. NRAS activity is modulated by interacting factors including NF1 (a GTPase-activating protein), SHOC2, and RASGAP. Disruption of Nras in this cell line abrogates these signaling axes, thereby attenuating proliferation and survival signals.
In the context of LLC lung carcinoma cells, Nras knockout creates a critical tool for studying RAS-dependent oncogenic processes. NRAS mutations are implicated in various cancers, including lung cancer, melanoma, and leukemia. By eliminating NRAS function, researchers can assess the contribution of RAS signaling to tumor growth, metastasis, and drug resistance. This model is especially relevant for investigating the dependency of lung cancer cells on MAPK and PI3K pathway activity, and for exploring synthetic lethality or compensatory signaling mechanisms that emerge upon RAS pathway inactivation.
The Nras Knockout LLC Cell Line supports a broad spectrum of experimental applications, including oncogenic signaling studies, drug sensitivity and resistance screening, and tumor microenvironment interaction analyses. Representative assays compatible with this model include western blotting for phospho-ERK and phospho-AKT to monitor pathway activity, cell proliferation assays (MTT, BrdU), flow cytometry for apoptosis, and cell migration and invasion assays. Additionally, the line can be employed in colony formation assays and xenograft tumor growth studies to evaluate tumorigenic potential in vivo. For further technical inquiries and detailed protocols, please contact Ascent Research.
