The AXL Knockout HCT 116 Polyclonal Cells product provides a CRISPR/Cas9-edited polyclonal population of HCT 116 human colorectal carcinoma cells harboring a disrupted AXL gene. This engineered cell model enables loss-of-function analysis of AXL, a receptor tyrosine kinase frequently implicated in tumor progression and therapy resistance. The polyclonal nature of the knockout pool preserves genetic diversity, allowing robust assessment of AXL-dependent phenotypes without clonal isolation artifacts. Cells are provided as a ready-to-use population for immediate functional studies.
The host HCT 116 cell line is an epithelial colorectal carcinoma model characterized by microsatellite instability (MSI), a KRAS G13D mutation, and wild-type TP53. These genetic features make HCT 116 particularly relevant for investigating oncogenic signaling networks in colorectal cancer. The cell line is extensively used to study tumorigenesis, metastatic behavior, and pharmacological responses to chemotherapeutic and targeted agents. The AXL knockout in this background permits dissection of AXL-specific contributions within a well-defined colorectal cancer framework.
AXL is a member of the TAM receptor tyrosine kinase family and functions as a high-affinity receptor for the ligand Gas6. Ligand binding triggers autophosphorylation and recruitment of adaptor proteins such as GRB2 and PI3K p85, leading to activation of the PI3K/AKT/mTOR and MAPK/ERK cascades. AXL signaling also converges on NF-??B and STAT3 transcriptional programs, driving expression of anti-apoptotic factors (BCL-2, MCL-1) and EMT regulators (Snail, ??-catenin). Crosstalk with other receptors, including EGFR, MET, and PDGFR, amplifies downstream signaling and contributes to adaptive resistance mechanisms. Upstream regulators include hypoxia (HIF-1??), inflammatory cytokines (IL-6, IL-10), and EGF, which transcriptionally upregulate AXL expression in tumor microenvironments.
In the HCT 116 colorectal carcinoma context, AXL knockout provides a powerful tool to interrogate its role in tumor cell survival, invasive migration, and drug insensitivity. Given the KRAS-mutant background, this model is particularly suited for examining AXL-mediated bypass signaling that sustains MAPK pathway activity and limits the efficacy of MEK or EGFR inhibitors. Disruption of AXL likely attenuates EMT-associated transcriptional programs and diminishes NF-??B-driven survival signals, offering insights into mechanisms of metastasis and immune evasion. The model thus bridges receptor tyrosine kinase signaling with colorectal cancer pathology.
Researchers can utilize the AXL Knockout HCT 116 Polyclonal Cells in a variety of functional assays, including Western blot analysis of AXL and downstream phospho-proteins (AKT, ERK), RT-qPCR for AXL mRNA quantification, cell proliferation (MTT) and Transwell migration assays, and flow cytometric assessment of apoptosis (Annexin V). This knockout model is also applicable in drug sensitivity profiling, AXL inhibitor screening, and in vivo tumor xenograft studies to evaluate tumor growth and metastatic dissemination. For further product details and technical support, please contact Ascent Research.
