The CARM1 Knockout PANC-1 Cell Line is a CRISPR/Cas9-edited knockout cell line engineered to disrupt the gene encoding coactivator-associated arginine methyltransferase 1 (CARM1) in the human pancreatic ductal adenocarcinoma PANC-1 background. This loss-of-function model provides a stable, ready-to-use cellular system for interrogating the epigenetic and transcriptional roles of CARM1 without the need for transient silencing approaches. The knockout cell line is suitable for a broad range of molecular and cellular analyses, enabling researchers to dissect CARM1-dependent mechanisms in a disease-relevant context.
PANC-1 is a widely employed epithelial cell line derived from a primary pancreatic ductal adenocarcinoma of a 56-year-old male. It retains hallmark features of pancreatic cancer, including oncogenic KRAS and TP53 mutations, and exhibits a poorly differentiated, highly invasive phenotype. This cell line serves as a robust model for studying pancreatic cancer biology, metastasis, and therapeutic responses. Its established use in academic and pharmaceutical research makes it an ideal host for gene-targeting studies, allowing direct assessment of gene function in a tumorigenic background.
CARM1 functions as a type I protein arginine methyltransferase that catalyzes asymmetric dimethylation of histone H3 at arginine 17 and 26 (H3R17me2a, H3R26me2a), thereby promoting transcriptional activation. It acts as a coactivator for a range of transcription factors, including p53, nuclear receptors, and NF-??B, and interacts with p300/CBP, SRC-3, MED1, and BRG1 to coordinate chromatin remodeling and mRNA splicing. CARM1 is activated downstream of AKT1 and PKC, and it regulates key targets such as CCND1, MMP9, BAX, and PUMA, linking arginine methylation to cell cycle progression, apoptosis, and epithelial-mesenchymal transition. Its activity integrates signals from p53, NF-??B, androgen receptor, and estrogen receptor pathways.
In the PANC-1 pancreatic cancer context, knockout of CARM1 eliminates its methyltransferase function, leading to loss of histone H3R17 and H3R26 methylation and subsequent disruption of coactivator-dependent transcriptional programs. This results in suppressed expression of proliferative and invasive genes like CCND1 and MMP9, while upregulating apoptotic effectors such as BAX and PUMA. Consequently, CARM1-depleted PANC-1 cells display reduced proliferation, impaired migration, and enhanced apoptosis, highlighting the enzyme??s critical role in maintaining pancreatic cancer cell aggressiveness. The model thus offers a physiologically relevant platform to study how arginine methylation drives oncogenic phenotypes.
Researchers can apply this knockout cell line to a variety of investigations, including epigenetic regulation in cancer, transcriptional control mechanisms, and pancreatic cancer biology. Typical assays include western blotting for CARM1 and methylated arginine marks, RT-qPCR quantification of target genes (e.g., CCND1, MMP9, BAX), MTT or other proliferation assays, transwell migration assays, Annexin V-based apoptosis detection, ChIP-qPCR for histone methylation status, and RNA-seq transcriptome profiling. The system is also suitable for drug target validation and metastasis research. For additional details or to inquire about this product, please contact Ascent Research.
