In Stock Cell Lines
Homo sapiens (Human)
Liver
Adherent
The MIR143 Knockout Hep-G2 Cell Line is a CRISPR/Cas9-edited knockout cell line derived from human hepatocellular carcinoma Hep-G2 cells, offering a loss-of-function model for the tumor-suppressive microRNA miR-143. This cell line enables investigation of miR-143??s role in regulating oncogenic pathways through direct silencing of targets such as KRAS and BCL2. Typical applications include miRNA tumor suppressor studies, drug target validation, and anti-cancer screening, using assays like proliferation, apoptosis, and migration analyses. It serves as a critical tool for liver cancer research and therapeutic development.
CAPN1 Knockout Raji Polyclonal Cells
Cat. No. ARG21475
Human Chondrocytes
Cat. No. ARP1032
ACAD10 Knockout MES-OV Polyclonal Cells
Cat. No. ARG24014
GPR108 Knockout AGS Polyclonal Cells
Cat. No. ARG26873
MAPKAPK2 Knockout HCT116 Polyclonal Cells
Cat. No. ARG7026
Rat Skeletal Muscle Cells
Cat. No. ARP0316
The MIR143 Knockout Hep-G2 Cell Line is a CRISPR/Cas9-edited knockout cell line derived from the human hepatocellular carcinoma Hep-G2 cell line, providing a loss-of-function model for the tumor-suppressive microRNA miR-143. Targeted disruption of the MIR143 locus enables study of miR-143-dependent regulatory mechanisms in liver cancer cells.
The parental Hep-G2 cell line, established from a male hepatocellular carcinoma patient, exhibits adherent epithelial morphology and retains hepatic functions including liver-specific protein expression and drug metabolism enzymes, making it a standard model for hepatic metabolism, drug toxicity, and hepatocarcinogenesis. This knockout line preserves host characteristics while permitting dissection of miR-143 function.
MIR143 encodes miR-143, a tumor suppressor microRNA that post-transcriptionally silences oncogenic mRNAs. Its expression is regulated by transcription factors such as p53 and KLF4, and its biogenesis requires DICER1/DGCR8 processing and RISC loading with AGO2. Mature miR-143 binds 3??UTRs of targets including KRAS, BCL2, MMP13, MYO6, and FNDC3B, leading to their suppression. This attenuates KRAS-driven MAPK/ERK and PI3K/AKT signaling, reducing ERK1/2 and AKT1 phosphorylation and BCL2 expression, thereby promoting apoptosis and inhibiting proliferation, migration, and invasion. MIR143 also interfaces with NF-??B and p53 pathways. Disruption of MIR143 abolishes these controls, enabling direct study of miR-143-dependent molecular mechanisms.
In hepatocellular carcinoma, miR-143 loss is common and linked to advanced disease and poor prognosis. This knockout line replicates that deficiency, allowing researchers to investigate consequences on cell cycle, apoptosis, and EMT. It is particularly useful for studying interactions with upstream regulators p53, KLF4, and NF-??B, and for validating downstream effectors like KRAS and BCL2. As an isogenic model, it enables rigorous dissection of miR-143 tumor-suppressive functions.
This cell line supports applications in miRNA biology, drug target validation, and anti-cancer screening. Moreover, the knockout line enables high-throughput screening of compounds that may restore miR-143 function or target downstream pathways. Functional assays include MTT proliferation, colony formation, Annexin V apoptosis, and transwell migration/invasion. Molecular analysis employs RT-qPCR for miR-143, western blotting for KRAS and BCL2, and reporter assays. Xenograft models assess tumorigenesis in vivo. For additional technical information, please contact Ascent Research.
