The ABHD6 Knockout CAL-27 Polyclonal Cells product comprises a population of CAL-27 human tongue squamous cell carcinoma epithelial cells in which the ABHD6 gene has been disrupted using CRISPR/Cas9 technology. These polyclonal knockout cells represent a heterogeneous pool of gene-edited cells, circumventing clonal selection artifacts and providing a robust loss-of-function model for ABHD6. This format is particularly suitable for bulk functional assays where the overall effect of target-gene disruption is assessed, and it enables researchers to study the gene??s role in oral cancer biology and endocannabinoid signalling.
The parental CAL-27 cell line was established from a primary tongue squamous cell carcinoma of a male patient and is widely employed as a model for oral cancer. CAL-27 cells exhibit characteristics of squamous cell carcinoma, including epithelial morphology and aggressive growth behaviour, and are used to investigate tumour cell proliferation, migration, invasion, and therapeutic response. The line provides a clinically relevant background for dissecting molecular pathways involved in oral carcinogenesis.
ABHD6 encodes a serine hydrolase that functions as a monoacylglycerol lipase, primarily catalysing the hydrolysis of 2-arachidonoylglycerol (2-AG), a major endocannabinoid, thereby terminating signalling at cannabinoid receptors CB1 and CB2. The enzyme is a key component of the endocannabinoid system and interacts with other lipid-metabolising enzymes such as monoacylglycerol lipase (MAGL), diacylglycerol lipase (DAGL) ??/??, and fatty acid amide hydrolase (FAAH). ABHD6 activity modulates several downstream pathways, notably MAPK/ERK and PI3K/AKT, and influences COX-2-dependent production of prostaglandin E2, linking lipid metabolism to inflammation and oncogenic signalling.
In the context of CAL-27 oral cancer cells, CRISPR/Cas9-mediated knockout of ABHD6 is expected to elevate intracellular 2-AG concentrations, leading to enhanced or prolonged CB1/CB2 receptor activation. This altered endocannabinoid signalling can impact critical cancer cell phenotypes such as proliferation, migration, and apoptosis, mediated through MAPK/ERK and PI3K/AKT cascades. The model thus enables detailed investigation of ABHD6??s role in oral squamous cell carcinoma and provides a platform to evaluate therapeutic strategies targeting endocannabinoid tone.
Researchers can employ these ABHD6 knockout polyclonal cells in diverse applications including oral cancer biology, endocannabinoid signalling studies, drug target validation, and cancer metabolism research. Typical assays include western blotting for ABHD6 and downstream signalling proteins (e.g., phosphorylated ERK, AKT), RT?qPCR for gene expression analysis, LC?MS quantification of 2?AG, MTT cell viability, wound healing migration, Transwell invasion, Annexin V/PI apoptosis, colony formation, CB1/CB2 receptor activity assays, and RNA?seq transcriptome profiling. For further information, please contact Ascent Research.
