The ERCC6L2-AS1 Knockout MIA PaCa-2 Cell Line is a CRISPR/Cas9-edited human pancreatic cancer model engineered to disrupt the ERCC6L2-AS1 gene, which encodes a long non?coding RNA antisense to the DNA repair?associated helicase ERCC6L2. This knockout cell line provides a stable loss?of?function system in the MIA PaCa?2 background, enabling precise interrogation of ERCC6L2?AS1 function without transient silencing artifacts. The CRISPR/Cas9?mediated gene disruption is introduced constitutively, generating a defined genetic tool suitable for reproducible functional genomics experiments, drug screening, and mechanistic studies of DNA damage response networks in pancreatic ductal adenocarcinoma.
The parental MIA PaCa?2 cell line is derived from the pancreatic tumor of a 65?year?old male with pancreatic adenocarcinoma and is established as a widely characterized model for pancreatic cancer biology. These cells harbor oncogenic KRAS G12C and TP53 mutations, rendering them particularly relevant for studies of tumorigenesis, metastasis, and therapeutic resistance. As pancreatic ductal adenocarcinoma epithelial cells, MIA PaCa?2 cells recapitulate key molecular features of the disease, including constitutive DNA replication stress and altered DNA repair capacity, which create a sensitized background for dissecting factors that maintain genomic stability.
ERCC6L2?AS1 is a long non?coding RNA that functionally interfaces with the DNA damage response and cell cycle regulatory networks. The lncRNA is regulated upstream by p53 and the stress?activated kinases ATM and ATR, positioning it as a downstream effector of the canonical DNA damage signaling cascade. ERCC6L2?AS1 modulates the expression of ERCC6L2 mRNA and other DNA repair effectors, potentially acting through physical interactions with the ERCC6L2 transcript, RNA?binding proteins, and chromatin?modifying complexes. Within the broader signaling framework, ERCC6L2?AS1 connects to pathway components such as CHEK1, CHEK2, H2AX, and BRCA1, suggesting its involvement in coordinating repair pathway choice and checkpoint activation.
In the TP53?mutant, KRAS?driven MIA PaCa?2 context, disruption of ERCC6L2?AS1 is predicted to impair DNA repair efficiency, leading to accumulation of unrepaired DNA lesions and enhanced susceptibility to genotoxic stress. This phenotype makes the knockout cell line a powerful tool for investigating lncRNA?mediated regulation of DNA damage responses in a disease?relevant setting, particularly for exploring mechanisms of chemoresistance and identifying synthetic lethality interactions that may be exploited therapeutically. The model also facilitates studies of how non?coding RNAs integrate with p53?independent DNA damage pathways in pancreatic cancer.
This product supports a wide range of experimental applications, enabling functional characterization of ERCC6L2?AS1 through assays such as western blotting for ??H2AX, RT?qPCR for gene expression profiling, and immunofluorescence detection of DNA repair foci. The cell line is well?suited for cell viability and clonogenic survival assays following treatment with DNA?damaging chemotherapeutics, comet assay to quantify DNA strand breaks, and cell cycle analysis by flow cytometry. Additionally, RNA immunoprecipitation can be used to identify protein or RNA interaction partners of the lncRNA. These applications make the product valuable for academic and pharmaceutical researchers studying pancreatic cancer biology, DNA repair deficiency syndromes, and non?coding RNA function. For further technical information, please contact Ascent Research.
