The ACER1 Knockout A2780 Polyclonal Cells constitute a CRISPR/Cas9-edited pool of A2780 ovarian carcinoma cells carrying disruptions in the ACER1 gene. This polyclonal population avoids clonal artifacts and provides a robust loss-of-function model for pooled functional studies, drug screens, and signaling analyses across heterogeneous genetic backgrounds.
The A2780 cell line, derived from an untreated ovarian cancer patient, is a standard model for studying high-grade serous carcinoma biology. Its adherent growth, TP53-mutant background, and extensive characterization in proliferation, apoptosis, and drug resistance research make it a practical host for genetic perturbation.
ACER1 encodes an alkaline ceramidase that hydrolyzes ceramides to sphingosine and free fatty acids, balancing pro-apoptotic ceramide and mitogenic sphingosine-1-phosphate (S1P). Regulated by upstream signals including TP53, PPARG, TNF, and IL1B, ACER1-generated sphingosine is phosphorylated by SPHK1/2 to S1P, which activates AKT1 and MAPK1 via S1P receptors. Ceramide synthases (CERS1-6) and other ceramidases interact with ACER1 to maintain sphingolipid homeostasis, placing ACER1 at a critical node controlling apoptosis through BCL2 family members and caspases.
In A2780 cells, ACER1 knockout is expected to elevate ceramide, sensitizing cells to apoptosis and attenuating AKT/MAPK prosurvival signaling. This model is especially relevant for dissecting ceramide-mediated cell death and overcoming chemoresistance, a major hurdle in ovarian cancer therapy.
Applications include mechanistic studies of sphingolipid signaling, ceramide-induced apoptosis, and therapy screening. The cells support Western blotting for ACER1, SPHK1, AKT, and MAPK; lipidomics by LC-MS/MS; caspase and Annexin V assays; and proliferation, migration, and drug sensitivity tests. For more information, contact Ascent Research.
