The ABHD6 Knockout T-47D Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population in which the ABHD6 gene has been disrupted to create a loss-of-function model. Supplied as a heterogeneous pool of gene-edited T-47D cells, this format avoids clonal selection biases while maintaining uniform target-gene ablation, providing a robust experimental system for studying ABHD6-dependent functions in breast cancer biology.
The parental T-47D cell line was established from a pleural effusion of a human mammary ductal carcinoma and serves as a widely used model of hormone-responsive breast cancer. These epithelial cells are ER+/PR+/HER2-, recapitulating the most common clinical breast cancer subtype, and exhibit estrogen-dependent growth, making them particularly relevant for investigating crosstalk between endocannabinoid signaling and hormone-driven tumor pathways.
ABHD6 encodes a 2-arachidonoylglycerol (2-AG) hydrolase that catalyzes the hydrolysis of 2-AG to arachidonic acid and glycerol. By controlling 2-AG availability, ABHD6 modulates cannabinoid receptor 1 (CB1) and CB2 activation, thereby regulating MAPK/ERK and PI3K/AKT signaling. Its activity is coordinated with the endocannabinoid enzymes monoacylglycerol lipase (MAGL), fatty acid amide hydrolase (FAAH), and diacylglycerol lipase alpha (DAGL??), and ABHD6 expression is regulated by peroxisome proliferator-activated receptor ?? (PPAR??), hypoxia-inducible factor 1-alpha (HIF-1??), and estrogen receptor.
In T-47D cells, ABHD6 knockout disrupts endocannabinoid tone by impairing 2-AG hydrolysis, leading to elevated 2-AG levels and sustained cannabinoid receptor engagement. This alteration can aberrantly activate MAPK/ERK and AKT, potentially affecting cell proliferation, survival, and hormone responsiveness. Concomitant reductions in arachidonic acid may diminish pro-inflammatory lipid mediator synthesis via cyclooxygenase-2 (COX-2). The knockout model thus provides a powerful tool to dissect ABHD6??s role in ER+ breast cancer cell adaptation, tumor progression, and metabolic signaling.
This ABHD6 knockout T-47D polyclonal cell population is ideally suited for functional genomics, endocannabinoid research, and drug discovery programs targeting lipid metabolism in hormone-responsive cancers. Researchers can employ Western blotting and RT-qPCR to confirm ABHD6 disruption, LC-MS to quantify 2-AG accumulation, and MTT or Annexin V assays to evaluate proliferation and apoptosis. Phospho-AKT/ERK signaling arrays and estrogen receptor reporter assays enable pathway analysis, while Transwell assays assess migration and invasion. Applications include studying drug resistance, metabolic reprogramming, and cancer signaling crosstalk. For further details, please contact Ascent Research.
