The MIR31 Knockout IPEC-J2 Cell Line is a CRISPR/Cas9-edited knockout cell line derived from porcine intestinal epithelial IPEC-J2 cells, engineered to disrupt the MIR31 gene encoding microRNA-31 (miR-31). This model abolishes miR-31-mediated post-transcriptional silencing, enabling study of de-repressed target mRNAs and downstream effects on proliferation, apoptosis, and inflammatory signaling. Applicable to cancer biology, inflammatory bowel disease, and epithelial barrier research.
The parental IPEC-J2 line is a non-transformed, differentiated porcine jejunal epithelial cell line maintaining polarized monolayer formation, tight junctions, and enterocyte-specific functions. It serves as an authentic in vitro model for swine intestinal barrier integrity, nutrient transport, and immune responses. Its retention of epithelial characteristics ensures physiological relevance for gene-edited derivatives used in host-microbe interaction and mucosal immunology studies.
miR-31 post-transcriptionally represses target mRNAs by binding 3??UTRs, with validated targets including tumor suppressors LATS2 and PPP2R2A, adaptor DOCK1, hydroxylase FIH-1, and Wnt antagonist DKK1. Its expression is induced by NF-??B, STAT3, IL-6, and hypoxia, and it functions within the RISC via AGO2 and TNRC6A. Consequently, miR-31 influences NF-??B (IKK??/??, I??B??, p65), Wnt/??-catenin (??-catenin, TCF4), MAPK/ERK, PI3K/Akt, and JAK-STAT pathways, thereby regulating proliferation, apoptosis, and inflammatory responses.
In IPEC-J2 cells, MIR31 knockout derepresses target mRNAs, potentially strengthening barrier integrity and attenuating inflammation. Relief of LATS2 and PPP2R2A repression promotes cell cycle arrest, while reduced DKK1 silencing enhances Wnt-driven epithelial renewal. Loss of miR-31??s inhibition on NF-??B components may modulate innate immune responses. This cell line enables dissection of miR-31??s role in tight junction regulation, cytokine signaling, and epithelial homeostasis under pathological challenges.
This cell line supports intestinal barrier studies via TEER and junctional immunofluorescence, inflammatory signaling analyses by Western blotting, ELISA, and flow cytometry, and host-microbe interaction assays. It is suitable for cancer biology (colorectal, gastric), drug transport/permeability assays, and combined with dual-luciferase reporter assays and RNA-seq for transcriptome-wide insights. For additional information, technical support, or custom inquiries, please contact Ascent Research.
