The LACTB2 Knockout HT29 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population derived from HT29 human colorectal adenocarcinoma cells. This product offers a loss-of-function model for the mitochondrial endoribonuclease LACTB2, enabling functional studies in a genetically diverse population without clonal artifacts.
HT29 cells originate from a primary colorectal adenocarcinoma of a 44-year-old female and serve as a well-characterized model of intestinal epithelial biology. Widely used in colon cancer research, they recapitulate aspects of tumor cell proliferation, differentiation, and metabolic adaptation. Their employment as a knockout background permits the dissection of gene function in a colorectal cancer-relevant cellular environment.
LACTB2 functions as a mitochondrial endoribonuclease involved in processing and degrading mitochondrial RNA. Its expression is regulated by key transcription factors and coactivators including TFAM, NRF1, NRF2, and PGC-1??. Within the mitochondrial RNA metabolism machinery, LACTB2 interacts with SUPV3L1, PNPT1, and mitochondrial ribosome proteins to modulate the processing of mitochondrial tRNAs, rRNAs, and mRNAs. This activity is essential for the proper expression of mitochondrial-encoded respiratory chain subunits and overall oxidative phosphorylation.
In colorectal cancer cells like HT29, mitochondrial function strongly influences metabolic programs and cell survival. Disruption of LACTB2 is expected to impair mitochondrial RNA processing, leading to reduced respiratory chain capacity and altered energy metabolism. This knockout model therefore provides a platform to study how defects in mitochondrial gene expression intersect with oncogenic pathways, potentially identifying vulnerabilities that can be exploited therapeutically.
These polyclonal LACTB2 knockout cells are suited for investigating mitochondrial RNA metabolism in colorectal cancer, examining the functional interactions of LACTB2 with PNPT1 and SUPV3L1, and conducting chemical screens for modulators of mitochondrial gene expression. Complementary assays include RT-qPCR analysis of mitochondrial transcripts, immunoblotting of respiratory chain subunits, mitochondrial respiratory complex activity measurements, cell proliferation and apoptosis assays, and RNA-seq profiling of mitochondrial RNA species. For additional details or assistance with experimental design, contact Ascent Research.
