The BPGM Knockout HeLa Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population designed for loss-of-function studies of the BPGM gene. Generated from the HeLa host cell line, this product comprises a genetically heterogeneous pool of cells, each carrying distinct CRISPR-induced mutations at the BPGM locus. This polyclonal approach avoids the selective pressures and clonal artifacts that can arise during single-cell cloning, thus providing a more representative model of gene disruption for functional genomics and metabolic investigations.
HeLa cells are a human epithelial cell line derived from HPV18-positive cervical adenocarcinoma, serving as a foundational model in cancer biology, virology, and cellular metabolism research. Their robust growth, well-characterized genome, and extensive use in assays make them an ideal platform for interrogating metabolic pathways. HeLa cells exhibit pronounced glycolytic activity and rapid proliferation, which are hallmarks of cervical cancer and epithelial tumor models, enabling detailed analysis of metabolic enzyme contributions to tumor cell adaptation and energy homeostasis.
The BPGM gene encodes bisphosphoglycerate mutase, a bifunctional enzyme central to the Rapoport-Luebering shunt. BPGM catalyzes the conversion of 1,3-bisphosphoglycerate to 2,3-bisphosphoglycerate (2,3-BPG) and its degradation to 3-phosphoglycerate. In erythroid cells, BPGM synthesizes 2,3-BPG to reduce hemoglobin oxygen affinity; in non-erythroid HeLa cells, it modulates glycolytic intermediate metabolism and energy status. Transcription is regulated by GATA1, induced by hypoxia, and acts downstream of erythropoietin signaling. BPGM forms a homodimer that binds bisphosphoglycerate, coordinating with glycolysis and gluconeogenesis to influence 3-phosphoglycerate, 1,3-BPG, and 2,3-BPG levels, thereby affecting cellular oxygen sensing and metabolic flux.
In the HeLa cervical adenocarcinoma background, BPGM knockout provides a valuable tool to dissect the non-canonical functions of the bisphosphoglycerate shunt. HeLa cells rely heavily on glycolysis for ATP production and biosynthetic intermediates, a phenomenon known as the Warburg effect. Disruption of BPGM may perturb the balance of glycolytic intermediates, 2,3-BPG levels, and metabolic adaptation to hypoxia, potentially affecting cell proliferation and survival. The polyclonal nature of this knockout product minimizes the impact of off-target effects and clonal variation, ensuring that observed phenotypes are attributable to BPGM loss rather than random genetic drift. This model is particularly relevant for exploring how metabolic enzyme dysregulation contributes to cancer progression, redox control, and therapeutic resistance in epithelial tumors.
This BPGM knockout model supports research in cancer metabolism, hypoxia response, glycolysis regulation, and non-erythroid 2,3-BPG function. Validation can be performed using Western blot for protein loss, RT-qPCR for transcript reduction, and RNA-seq for transcriptome profiling. Functional analyses include enzyme activity assays, 2,3-BPG quantification, cell proliferation under normoxia/hypoxia, and metabolic flux analysis. Hypoxia exposure experiments enable study of HIF-mediated adaptation. For further information, contact Ascent Research.
