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.
CAMK2G Knockout Hela Polyclonal Cells
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C2orf69 Knockout HGC-27 Polyclonal Cells
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P4HTM Knockout NCI-H1299 Polyclonal Cells
Cat. No. ARG17551
CRELD1 Knockout jurkat Polyclonal Cells
Cat. No. ARG13077
MTHFD2 Knockout SKOV3 Polyclonal Cells
Cat. No. ARG12411
LRRC59 Knockout Hela Polyclonal Cells
Cat. No. ARG9001
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.
