The CCDC90B Knockout SK-HEP-1 Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal cell population in which the CCDC90B gene has been disrupted in the human hepatic adenocarcinoma cell line SK-HEP-1. This product provides a heterogeneous pool of gene-edited cells, generated by transient expression of Cas9 and a guide RNA targeting CCDC90B, to create a functional knockout model without single-cell cloning. The resulting polyclonal population enables researchers to investigate the consequences of CCDC90B loss in a near-native cellular context, minimizing clonal artifacts.
SK-HEP-1 is a widely used human hepatic adenocarcinoma cell line originally derived from the ascitic fluid of a patient with liver adenocarcinoma. Despite its hepatic origin, SK-HEP-1 cells exhibit endothelial-like morphology and functional characteristics, making them a versatile model for studying tumor biology, angiogenesis, and drug responses. The cell line is commonly employed in hepatocarcinoma research and preclinical drug screening due to its reproducible growth and well-characterized signaling networks.
CCDC90B encodes a mitochondrial coiled-coil domain-containing protein implicated in the regulation of mitochondrial calcium (Ca2?) uptake and apoptotic signaling. Functionally, CCDC90B interacts with the mitochondrial calcium uniporter (MCU) complex, including MICU1, and modulates the activity of the permeability transition pore by influencing BCL-2 and BAX dynamics. Its knockout disrupts mitochondrial Ca2? buffering, leading to altered cytochrome c release and downstream caspase-9 and caspase-3 activation. Upstream, CCDC90B expression is regulated by mitochondrial biogenesis factors such as PGC-1?? and NRF1, and is responsive to AMPK-mediated metabolic cues. Thus, CCDC90B acts as a node linking metabolic signals to cell fate decisions.
In the SK-HEP-1 hepatic adenocarcinoma background, CCDC90B knockout presents a valuable model for dissecting the interplay between mitochondrial calcium signaling and tumor cell survival. Loss of CCDC90B is expected to sensitize cells to apoptotic stimuli by diminishing mitochondrial Ca2?-dependent activation of pro-survival pathways, thereby providing insights into mechanisms of drug resistance in hepatocellular carcinoma. Moreover, this model facilitates the study of mitochondrial permeability transition and its role in metabolic reprogramming, a hallmark of cancer cells.
This polyclonal knockout cell product is well-suited for a range of experimental applications, including mitochondrial calcium imaging using Rhod-2 AM, apoptosis profiling via Annexin V/PI flow cytometry, and functional metabolic assays such as Seahorse extracellular flux analysis. It supports co-immunoprecipitation studies to investigate CCDC90B interactions with MCU and BCL-2 family proteins, as well as Western blotting and RT-qPCR to assess downstream effector activation. Researchers can utilize this model in drug screening campaigns targeting mitochondrial apoptosis in hepatic adenocarcinoma, or in mechanistic studies of mitochondrial calcium handling and cell death regulation. For additional information or technical support, please contact Ascent Research.
