The ALOX12 Knockout CAL-27 Polyclonal Cells constitute a CRISPR/Cas9-edited polyclonal knockout cell population designed for targeted disruption of the ALOX12 gene in the human CAL-27 epithelial cell line. This product provides a heterogeneous loss-of-function model, enabling investigation of arachidonate 12-lipoxygenase (12-LOX) in cancer-relevant signaling networks. The polyclonal format offers a pooled population of knockout cells that maintains biological complexity while eliminating ALOX12-dependent functions, facilitating robust and reproducible studies in oral squamous cell carcinoma research.
The CAL-27 host cell line is derived from a human tongue squamous cell carcinoma and represents a well-characterized model of oral cancer. These adherent epithelial cells exhibit an aggressive phenotype with high invasive and migratory properties, making them particularly suitable for functional genomics studies of metastasis and tumor progression. CAL-27 cells are widely employed in oncogenic signaling research, drug screening, and evaluation of tumor microenvironment interactions due to their relevance to head and neck malignancies.
ALOX12 catalyzes the conversion of arachidonic acid, provided by PLA2, to 12S?hydroperoxyeicosatetraenoic acid (12?HPETE), which is subsequently reduced to the lipid mediator 12?HETE. 12?HETE engages the BLT2 and GPR31 receptors, triggering phosphorylation of ERK1/2 and AKT and activation of MAPK and PI3K?AKT signaling. ALOX12 expression is controlled by upstream regulators including NF???B, AP?1, SP1, TNF???, IL?1??, EGF, and oxidative stress. Downstream, the 12?HETE?BLT2 pathway drives cyclin D1 expression and modulates transcription factors such as NF???B and p53, promoting proliferation, survival, and epithelial?mesenchymal transition. ALOX12 interacts with FLAP, PLA2, and platelet?activating factor acetylhydrolase within the eicosanoid network.
In the CAL-27 context, ALOX12 overexpression has been associated with enhanced tumor growth and metastasis, making its disruption a powerful tool for dissecting lipoxygenase-driven oncogenic mechanisms. This polyclonal knockout cell population allows researchers to assess how loss of 12?LOX activity affects key phenotypes such as colony formation, migration, invasion, and apoptosis. The model is especially relevant for studying the role of lipid mediators in oral squamous cell carcinoma progression, epithelial?mesenchymal transition, and therapy resistance, thereby supporting target validation studies for novel anti?cancer agents.
This product supports a broad range of experimental applications, including functional genomics of lipoxygenases, anti?cancer compound screening, and investigation of tumor microenvironment and metastasis. Users can employ complementary techniques such as western blotting, RT?qPCR, RNA?seq, lipidomics, flow cytometry, Transwell migration assays, wound healing assays, colony formation assays, and apoptosis detection to characterize the molecular and cellular consequences of ALOX12 deletion. The polyclonal cell population is suitable for both mechanistic studies and high-throughput drug screens. For further technical details or custom inquiries, please contact Ascent Research.
