The ABHD6 Knockout UM-UC-3 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population targeting the ABHD6 gene. This mixed-cell pool harbors heterogeneous gene disruptions that collectively abolish ABHD6 function, avoiding clonal selection biases. Validated and ready for use, the model enables population-level analyses in functional genomics and cancer biology.
The UM-UC-3 cell line derives from a male patient with bladder transitional cell carcinoma and is a well-established model for urothelial carcinoma. These adherent epithelial cells display aggressive properties, including tumorigenicity in xenografts and chemotherapeutic responsiveness. Frequently used to study bladder cancer tumorigenesis, metastasis, and drug resistance, UM-UC-3 provides a clinically relevant background for investigating ABHD6 in bladder cancer biology.
ABHD6 encodes a serine hydrolase that acts as a monoacylglycerol lipase, hydrolyzing the endocannabinoid 2-arachidonoylglycerol (2-AG) into arachidonic acid and glycerol. This activity regulates endocannabinoid tone and modulates signaling through CB1 and CB2 cannabinoid receptors. Transcription of ABHD6 is governed by PPAR?? and LXR, and its activity responds to nutrient status, linking lipid metabolism with cellular energy balance. By controlling 2-AG levels, ABHD6 influences downstream eicosanoid production from arachidonic acid and cell proliferation pathways. Other 2-AG hydrolases, including MAGL and FAAH, collaborate in a complex network that compartmentalizes endocannabinoid signaling.
Aberrant lipid signaling and metabolic reprogramming contribute to bladder cancer progression and therapy response. UM-UC-3 cells, with their tumorigenic traits, provide a suitable system to dissect ABHD6 function in urothelial carcinogenesis. ABHD6 disruption is predicted to elevate 2-AG levels, enhancing basal cannabinoid receptor activity and altering arachidonic acid?Cderived eicosanoid balance. These changes may affect proliferation, apoptosis, and invasion, enabling investigation of how endocannabinoid signaling intersects with cancer pathways. Additionally, given ABHD6??s links to metabolic disorders, this model can help bridge bladder cancer biology with systemic metabolic dysfunction.
These polyclonal knockout cells support Western blot, RT-qPCR, and lipidomics for verifying gene disruption and quantifying 2-AG by mass spectrometry. Functional assays include cell proliferation, migration, invasion, and flow cytometry for cell cycle analysis. Xenograft studies enable in vivo assessment of tumorigenic potential, while drug sensitivity testing evaluates synthetic lethal interactions. The model is valuable for endocannabinoid signaling research, cancer metabolism studies, and bladder cancer lipid biology. For further details or custom gene-editing requests, please contact Ascent Research.
