The ACSS2 Knockout TE1 Polyclonal Cells product comprises a polyclonal population of TE1 esophageal squamous carcinoma cells engineered by CRISPR/Cas9 to disrupt the ACSS2 gene. This heterogeneous knockout model avoids clonal artifacts and faithfully represents the functional consequences of ACSS2 loss across a diverse edited pool.
Derived from a human esophageal squamous cell carcinoma, the TE1 cell line exhibits adherent epithelial morphology and serves as a well-characterized model for esophageal cancer research. TE1 cells retain metabolic and oncogenic properties relevant to the tumor type, making them an appropriate host for interrogating ACSS2 function in a malignant epithelial context.
ACSS2 converts acetate to acetyl-CoA, a key substrate for lipid synthesis and histone acetylation. Its expression is driven by SREBP1 and HIF-1?? and regulated by AMPK signaling. The resulting acetyl-CoA is utilized by FASN and ACC for de novo lipogenesis and by histone acetyltransferases like CBP/p300 to acetylate H3K27, modulating chromatin structure. ACSS2 interacts with ACLY, FASN, ACC, and TFEB, placing it at the intersection of metabolic and epigenetic control networks. Under conditions of limited nutrient availability, ACSS2-mediated acetate recycling becomes a critical anapleurotic route for acetyl-CoA production, influencing both lipid droplet formation and the epigenetic landscape.
In esophageal squamous cell carcinoma, the acetate-to-acetyl-CoA axis mediated by ACSS2 is critical for supplying lipid precursors and acetyl groups that support rapid proliferation and oncogenic transcription. The TE1 knockout model enables dissection of how ACSS2 loss affects tumor lipogenesis, acetate utilization, and histone acetylation marks such as H3K27ac. It provides a disease-relevant system to investigate the interplay between hypoxia (HIF-1??), energy sensing (AMPK), and acetyl-CoA metabolism in aggressive esophageal cancer phenotypes.
This polyclonal knockout product supports diverse assays including RNA-seq, ChIP-qPCR for H3K27ac, lipid droplet staining, acetate uptake measurements, and oxygen consumption rate (OCR) analysis to characterize metabolic and epigenetic outcomes. Western blotting for ACSS2 and downstream effectors like FASN validates knockout and pathway engagement. Applications extend to acetate tracing for carbon flux analysis, lipogenesis inhibition, and exploring ACSS2 as a vulnerability in obesity-linked cancers and cachexia. Moreover, the cells can be deployed in co-culture systems or xenograft studies to assess the role of ACSS2 in tumor growth and metastatic potential. For additional details or assistance, contact Ascent Research.
