In Stock Cell Lines
Homo sapiens (Human)
Pancreas
Adherent
The EPB41L4A-AS1 Knockout PANC-1 Cell Line is a CRISPR/Cas9-edited knockout model targeting the long non-coding RNA EPB41L4A-AS1 in the human pancreatic ductal adenocarcinoma cell line PANC-1. EPB41L4A-AS1 functions as a ceRNA that sponges miR-214-3p to derepress glycolytic targets HK2 and LDHA, with its expression regulated by HIF-1?? and c-Myc. This knockout line is designed for investigating lncRNA-mediated metabolic reprogramming, miRNA interactions, and tumorigenic properties in pancreatic cancer. It supports functional assays such as Seahorse analysis, dual-luciferase reporter assays, Transwell migration, and CCK-8 proliferation.
DDX60 Knockout A2780 Polyclonal Cells
Cat. No. ARG18592
KCTD15 Knockout Raji Polyclonal Cells
Cat. No. ARG23884
ANTXR1 Knockout huh-7 Polyclonal Cells
Cat. No. ARG27908
KPNA3 Knockout HGC-27 Polyclonal Cells
Cat. No. ARG30149
DLGAP5 Knockout A549 Polyclonal Cells
Cat. No. ARG38928
NGLY1 Knockout HEK293T Cell Line
Cat. No. ARG0310
The EPB41L4A-AS1 Knockout PANC-1 Cell Line is a CRISPR/Cas9-edited knockout cell line targeting the long non-coding RNA EPB41L4A-AS1 in the human PANC-1 pancreatic ductal adenocarcinoma cell line. EPB41L4A-AS1 is an antisense transcript that functions as a competing endogenous RNA (ceRNA) and participates in chromatin remodeling, thereby regulating gene expression networks involved in cell proliferation, migration, and invasion. This loss-of-function model provides a stable and reproducible system for dissecting the molecular roles of EPB41L4A-AS1 in cancer biology.
The parental PANC-1 cell line is derived from a human pancreatic ductal adenocarcinoma and harbors an activating KRAS G12D mutation along with TP53 mutation, representing a genetically defined model of aggressive pancreatic cancer. As an epithelial cancer cell line, PANC-1 is extensively used to study tumor invasion, metastasis, and metabolic adaptation. This genetic background offers a clinically relevant context to investigate EPB41L4A-AS1, which is frequently dysregulated in pancreatic malignancies.
EPB41L4A-AS1 acts primarily as a ceRNA that sponges miR-214-3p, thereby relieving repression of downstream targets including HK2, LDHA, and TGFBR1. Its expression is transcriptionally activated by HIF-1?? and c-Myc, integrating hypoxic and oncogenic signals to drive metabolic reprogramming and Wnt/??-catenin pathway activity. Additionally, EPB41L4A-AS1 interacts with the PRC2 complex (EZH2/SUZ12) and the RNA-binding protein HuR, linking it to epigenetic silencing and mRNA stability.
In PANC-1 cells, knockout of EPB41L4A-AS1 disrupts the ceRNA network, leading to increased miR-214-3p activity and consequent suppression of HK2 and LDHA. This impairs aerobic glycolysis, reduces ??-catenin signaling, and attenuates tumorigenic properties such as proliferation, migration, and invasion. Thus, the knockout model recapitulates a loss-of-function phenotype that underscores the functional importance of EPB41L4A-AS1 in pancreatic cancer aggressiveness.
Researchers can apply this cell line in transcriptomic studies via RNA-seq and RT-qPCR, validate miRNA-lncRNA interactions using dual-luciferase reporter assays, and assess metabolic reprogramming with Seahorse extracellular flux analysis. Functional readouts include Transwell migration/invasion assays, CCK-8 proliferation assays, and flow cytometry for apoptosis. The model also supports drug screening targeting the HIF-1??/c-Myc/EPB41L4A-AS1 axis. For further inquiries, please contact Ascent Research.
