The ACER1 Knockout CAL-27 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human CAL-27 oral squamous cell carcinoma cell line. This product features disruption of the ACER1 gene using a non-viral CRISPR/Cas9 ribonucleoprotein delivery method, resulting in a heterogeneous pool of cells with targeted loss-of-function mutations. As a polyclonal population, it captures a range of editing outcomes and is well-suited for experiments where maintaining genetic diversity or avoiding clonal artifacts is desired.
The parental CAL-27 line was established from a tongue squamous cell carcinoma lesion of a 56-year-old male patient and has become a standard model in oral cancer research. These epithelial cells exhibit adherent growth, harbor TP53 mutations, and display hallmark characteristics of aggressive carcinoma, including rapid proliferation and invasive potential. CAL-27 is widely employed to investigate molecular mechanisms of oral carcinogenesis, response to therapeutics, and tumor-stroma interactions.
ACER1 encodes an alkaline ceramidase that hydrolyzes ceramides to sphingosine and free fatty acids, thereby controlling the balance between proapoptotic ceramides and sphingosine-derived sphingosine-1-phosphate (S1P). This enzyme is activated by upstream signals such as TNF-??, p53, and cellular stress, and its activity generates sphingosine, which is subsequently phosphorylated by sphingosine kinases to form S1P. S1P signals through S1P receptor 1 to activate downstream kinases AKT and ERK, while ceramides engage protein phosphatases and Bcl-2 family members to promote apoptosis. ACER1 thus functions as a critical node coordinating cell fate decisions within sphingolipid metabolism.
In the context of oral squamous cell carcinoma, ACER1 gene disruption in CAL-27 cells leads to abnormal accumulation of ceramide species and reduced sphingosine availability. This perturbation favors ceramide-driven apoptotic signaling over S1P-mediated survival and proliferation pathways, potentially sensitizing the cells to apoptotic stimuli, inhibiting AKT/ERK-dependent growth signals, and altering migratory and invasive properties. The polyclonal knockout model therefore enables detailed investigation of how ACER1 loss contributes to tumor progression and response to microenvironmental cues in a genetically representative cancer background.
Researchers can utilize this product to quantify changes in sphingolipid metabolites via mass spectrometry and S1P ELISA, measure apoptosis induction with annexin V staining, assess cell viability through MTT assay, and monitor signaling events by western blotting for phosphorylated AKT and ERK. Additional functional assays, including migration and invasion studies, further elucidate the role of ACER1 in cancer cell behavior. The polyclonal format is particularly advantageous for drug screens targeting sphingolipid pathway components such as sphingosine kinases or S1P receptors. For further information or technical assistance with the ACER1 Knockout CAL-27 Polyclonal Cells, please contact Ascent Research.
