ACER1 Knockout HGC-27 Polyclonal Cells provide a CRISPR/Cas9-edited polyclonal knockout cell population in which the ACER1 gene has been disrupted, resulting in a loss-of-function model for studying alkaline ceramidase activity. This product enables systematic investigation of sphingolipid metabolism in a human gastric carcinoma background by abrogating the conversion of ceramides to sphingosine and fatty acid. The polyclonal population preserves the heterogeneity of editing outcomes, making it suitable for pooled functional analyses without clonal selection artifacts.
The host cell line, HGC-27, is a human gastric epithelial cell line originally derived from the lymph node metastasis of a gastric adenocarcinoma. It serves as a well-characterized in vitro model for gastric cancer research, exhibiting features of epithelial origin and metastatic potential. HGC-27 cells retain key signaling pathways involved in gastric carcinogenesis, making them a relevant platform for dissecting the role of sphingolipid homeostasis in tumor progression.
ACER1 functions as a critical enzyme in the ceramide?Csphingosine?Csphingosine-1-phosphate (S1P) rheostat. It hydrolyzes ceramide substrates to produce sphingosine, which is rapidly phosphorylated by sphingosine kinases to generate the bioactive lipid S1P. Upstream regulators include cellular stress signals and inflammatory cytokines, while downstream targets comprise sphingosine-1-phosphate, sphingosine kinase 1, ceramide synthases, and BCL2 family proteins. Interacting factors include other ceramidases and ceramide substrates. In the knockout model, loss of ACER1 activity leads to ceramide accumulation and reduced generation of sphingosine and S1P, thereby shifting the balance toward pro-apoptotic ceramide signaling and away from survival and proliferation signals mediated by S1P receptors.
In the HGC-27 gastric cancer context, ACER1 knockout disrupts ceramide metabolism in a cell line with intrinsic metastatic characteristics. This model allows researchers to explore how altered sphingolipid flux influences apoptosis, cell proliferation, and migration in gastric adenocarcinoma. It is particularly valuable for studying the interplay between ceramide-induced stress responses and S1P-driven oncogenic pathways, and for evaluating therapeutic strategies that target sphingolipid enzymes.
Typical applications include quantitative analysis of ceramide species by LC-MS, measurement of sphingosine-1-phosphate by ELISA, and functional assays such as Annexin V/PI apoptosis detection, MTT proliferation assays, and scratch wound migration studies. Gene expression profiling via RT-qPCR for sphingolipid enzyme transcripts can complement these analyses. This knockout model is well-suited for drug target validation, pathway dissection, and phenotypic screening in gastric cancer research. For additional details, please contact Ascent Research.
