The ACSS2 Knockout LoVo Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the LoVo human colorectal adenocarcinoma cell line. This product provides a genetically disrupted ACSS2 gene across a heterogeneous cell population, enabling loss-of-function studies of acetyl-CoA synthetase short-chain family member 2 (ACSS2) without selection for a single clonal isolate.
The LoVo host cell line was established from a metastatic colon adenocarcinoma and displays epithelial morphology, making it a widely used model for colorectal cancer research. Its relevance to tumor progression, metastatic behavior, and therapeutic response makes LoVo an ideal background for investigating cancer metabolism pathways.
ACSS2 catalyzes the conversion of acetate to acetyl-CoA, a critical metabolite that feeds into both de novo lipogenesis and histone acetylation. This reaction is regulated by multiple upstream signals, including SREBP transcription factors, HIF-1?? under hypoxic conditions, AMPK, and insulin signaling, and is influenced by acetate availability. Downstream, ACSS2-generated acetyl-CoA expands the acetyl-CoA pool, serving as substrate for fatty acid synthase (FASN) in lipid synthesis and for histone acetyltransferases such as p300/CBP, which modulate histone acetylation and gene expression. ACSS2 thus functions downstream of metabolic sensors and upstream of lipogenic and epigenetic machinery. It also interacts with AMPK and homodimerizes, and is part of a pathway that includes ACLY, ACC, FASN, p300/CBP, HDACs, SREBP1, and HIF-1??, linking nutrient status to chromatin modification and lipid anabolism.
In the context of LoVo colorectal adenocarcinoma cells, ACSS2 plays an important role in metabolic reprogramming that supports rapid proliferation and survival under metabolic stress. The knockout model allows researchers to dissect how loss of ACSS2 impacts acetyl-CoA-dependent processes such as fatty acid synthesis and histone acetylation, providing insights into the metabolic dependencies of colorectal tumors. This model is particularly valuable for studying hypoxia-induced metabolic adaptation, as ACSS2 is upregulated by HIF-1?? and contributes to the epigenetic regulation of hypoxia-responsive genes.
Typical applications include investigating cancer metabolism, lipid metabolism, and epigenetics through assays such as acetyl-CoA quantification, 1?C-acetate incorporation for fatty acid synthesis, and histone acetylation ChIP-seq. Researchers can also assess cell proliferation, hypoxia response gene expression via RT-qPCR, and drug resistance mechanisms. The polyclonal nature of the knockout allows for studying population-level effects and heterogeneous responses. For additional information or to request a quote, please contact Ascent Research.
