The MLLT6 Knockout AGS Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population targeting the MLLT6 (AF17) gene in the human gastric adenocarcinoma AGS cell line. This product comprises a heterogeneous pool of cells with targeted gene disruption, generated via CRISPR/Cas9-mediated genome editing, without clonal isolation. It is optimized for functional genomics studies requiring a physiologically relevant gastric cancer model.
The AGS cell line is an adherent epithelial cell line isolated from a patient with gastric adenocarcinoma. It serves as a well-characterized in vitro model for gastric cancer research, retaining key features of the disease such as dysregulated proliferation and invasion. This host background enables the investigation of gene function in a gastric adenocarcinoma context.
MLLT6 encodes a core subunit of the super elongation complex (SEC), which releases paused RNA polymerase II (Pol II) into productive transcription elongation. Within the SEC, MLLT6 interacts with ELL, EAF1, EAF2, AFF1, AFF4, and bridges to the P-TEFb kinase complex (CDK9/cyclin T1). SEC activity is regulated by upstream factors including MLL1 fusion proteins and c-MYC, and it drives expression of downstream targets such as the HOXA gene cluster and c-MYC target genes. Disruption of MLLT6 impairs SEC assembly and function, leading to reduced Pol II Ser2 phosphorylation and diminished transcriptional elongation of these critical loci.
In gastric adenocarcinoma, aberrant transcriptional elongation may contribute to oncogenic gene expression. The MLLT6 knockout in AGS cells provides a direct loss-of-function model to dissect the SEC’s role in gastric cancer cell proliferation, survival, and invasion. Given MLLT6’s involvement in MLL-rearranged leukemogenesis, this model also facilitates cross-cancer comparisons of SEC-dependent transcriptional mechanisms.
These polyclonal knockout cells are suitable for a variety of research applications, including functional characterization of SEC complex dynamics, drug target validation, and CRISPR-based synthetic lethal screens. Representative assays include western blotting for MLLT6 and SEC components, RT-qPCR for HOXA9 and c-MYC, ChIP-qPCR for Pol II Ser2 phosphorylation, and functional assays such as MTT proliferation, Annexin V apoptosis, and transwell migration/invasion assays. RNA-seq can profile global transcriptomic changes upon MLLT6 loss. For additional information, please contact Ascent Research.
