The INHBE Knockout HGC-27 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human gastric carcinoma epithelial cell line HGC-27. This product features a targeted disruption of the INHBE gene using CRISPR/Cas9 technology, generating a heterogeneous pool of cells with loss-of-function mutations in the inhibin beta E subunit locus.
The HGC-27 cell line was originally established from the metastatic lymph node of a patient with gastric adenocarcinoma. These cells are tumorigenic and serve as a widely used model for studying gastric cancer progression, metastatic dissemination, and tumor?Cstroma interactions. Their epithelial origin and malignant properties make them particularly suitable for investigating signaling pathways that drive proliferation, invasion, and metabolic reprogramming in gastric carcinomas.
INHBE encodes the inhibin beta E subunit, an activin-like ligand within the TGF-?? superfamily. INHBE signals by binding to activin receptor complexes composed of ACVR1B and ACVR2A, leading to phosphorylation of the intracellular effectors SMAD2 and SMAD3. Phosphorylated SMAD2/3 partner with SMAD4 and translocate to the nucleus to regulate transcription of genes such as SERPINE1, CTGF, and MMP2/9, as well as metabolic enzyme genes. The cascade is modulated by upstream factors including TGF-?? ligands, transcription factors FOXO1 and HNF4A, metabolic signals (insulin, glucose), and inflammatory cytokines like TNF-??. INHBE also interacts with the inhibin alpha subunit and participates in crosstalk with MAPK/ERK and PI3K/AKT pathways, positioning it at the intersection of growth factor signaling and metabolic control.
Knockout of INHBE in HGC-27 cells disrupts this signaling axis, providing a powerful tool for dissecting the contribution of inhibin beta E to gastric cancer pathobiology. Because HGC-27 cells retain key features of metastatic adenocarcinoma, the INHBE loss-of-function model enables investigation into how altered TGF-??/activin?CSMAD signaling affects tumor cell proliferation, apoptosis, migration, and metabolic adaptation. This model is particularly relevant for studying the link between obesity-associated metabolic dysregulation and gastric cancer aggression, as INHBE has been implicated in metabolic syndrome and type 2 diabetes. The polyclonal nature of the knockout pool mimics heterogeneous tumor cell populations, offering a realistic cellular context for functional studies.
Researchers can employ these cells in a variety of assays, including western blotting to assess SMAD2/3 phosphorylation and INHBE expression, RT?qPCR for downstream target genes such as SERPINE1 and CTGF, proliferation and migration/invasion assays, metabolic flux measurements (glucose uptake, ATP levels), RNA?seq transcriptomic profiling, co?immunoprecipitation for receptor interactions, and phospho?signaling analysis. Typical applications encompass gastric cancer progression studies, metabolic regulation in cancer, TGF??? signaling dissection, drug target validation, and metastasis mechanism investigation. For further information or technical support, please contact Ascent Research.
