The ALOX12 Knockout TE1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal cell population derived from the human esophageal squamous cell carcinoma line TE1, with targeted disruption of the ALOX12 gene. This knockout model eliminates the production of 12-lipoxygenase, abrogating the synthesis of 12-HPETE and 12-HETE. Supplied as a polyclonal pool, these cells enable robust loss-of-function analyses without the need for single-cell cloning, providing a physiologically relevant tool for studying ALOX12-dependent processes in cancer.
TE1 is a well-differentiated human esophageal squamous cell carcinoma cell line that retains hallmark epithelial characteristics. It is widely used as a model for ESCC pathogenesis, supporting reproducible investigations into the molecular drivers of this malignancy. Its adherent morphology and stable growth make it suitable for gene editing and subsequent functional assays.
ALOX12 converts arachidonic acid to 12-HPETE and 12-HETE, a lipid second messenger. 12-HETE binds GPCRs, activating GNAQ, PLCB, and PRKCA, which leads to MAP2K1-MAPK1/3 (ERK) phosphorylation and induction of FOS and JUN. Upstream, ALOX12 is transcriptionally regulated by EGFR, TGFB1, IL1B, TNF, and factors SP1, AP-1, p53. Downstream, it modulates AKT and NF-??B (NFKB1) survival pathways, PPARG-mediated transcription, and the BAX/BCL2 apoptosis switch, while also promoting MMP9 expression and VEGF production. ALOX12 cooperates with ALOX5, PLA2G4A, CYP450s, and GPX4 in lipid metabolic networks.
In ESCC, ALOX12 overexpression is associated with increased proliferation, survival, and metastatic potential through sustained MAPK/ERK and NF-??B activation and upregulation of MMP9 and VEGF. Knockout of ALOX12 in TE1 cells abrogates 12-HETE-dependent signaling, predicting reduced tumorigenic properties, enhanced apoptosis, and attenuation of invasive behavior. This polyclonal knockout model enables dissection of the specific contributions of 12-lipoxygenase to ESCC biology.
These cells are suitable for target validation, signaling pathway analysis, and functional studies. Typical assays include immunoblotting for phospho-ERK and other effectors, cell proliferation and apoptosis measurements, migration and invasion assays, and 12-HETE ELISA for metabolic confirmation. Transcriptomic profiling (RNA-seq, RT-qPCR) can elucidate downstream gene networks. The model supports biomarker discovery, drug sensitivity screening, and exploration of crosstalk between MAPK, NF-??B, and PPAR?? pathways. For more information, contact Ascent Research.
