The IGFBP5 Knockout SK-HEP-1 Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout population targeting the human IGFBP5 gene in the SK-HEP-1 hepatic adenocarcinoma cell line. This loss-of-function model eliminates IGFBP5 protein expression, enabling functional studies of IGFBP5 in a liver tumor context. The polyclonal format provides a heterogeneous pool that can be used directly in assays or for subsequent clonal isolation.
SK-HEP-1 is a well-characterized human liver adenocarcinoma cell line extensively employed in hepatocellular carcinoma (HCC) research. It exhibits malignant properties such as anchorage-independent growth and tumorigenicity in vivo, making it a suitable platform for dissecting oncogenic signaling and metastatic mechanisms.
IGFBP5 encodes a secreted IGF-binding protein that regulates IGF-I and IGF-II bioavailability, thereby modulating downstream cascades including IGF1R?CPI3K?CAKT?CmTOR and RAS?CERK (involving AKT and ERK1/2). In addition, IGFBP5 exerts IGF-independent effects through interactions with thrombospondin-1, LRP1, and integrins. Its transcription is controlled by p53, TGF-??, glucocorticoids, and FOXO factors. IGFBP5 influences apoptosis via BAX, cell cycle arrest via p21, and migration via MMP-9, linking p53 and Wnt pathways to cellular responses.
In SK-HEP-1 cells, IGFBP5 knockout provides a means to study its role in HCC progression. Perturbation of IGFBP5 can alter apoptotic and proliferative signals, potentially impacting metastatic capacity and drug sensitivity. This model is valuable for investigating epithelial-to-mesenchymal transition, invasion, and the interplay between IGF and p53 pathways in liver cancer.
Applications include cancer biology, senescence, and fibrosis research. Typical experiments encompass proliferation and apoptosis assays, migration/invasion studies, colony formation, and wound healing, along with molecular techniques such as western blotting, RT-qPCR, co-immunoprecipitation, reporter assays, and RNA-seq. This product facilitates drug resistance studies and the identification of therapeutic targets in HCC. For additional information, please contact Ascent Research.
