The INHBE Knockout KYSE-150 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal cell population with targeted disruption of the INHBE gene in the KYSE-150 human esophageal squamous cell carcinoma line. This loss-of-function model enables study of INHBE-dependent pathways without single-cell clone bias, suitable for population-level analyses and high-throughput applications.
KYSE-150, derived from a poorly differentiated esophageal squamous cell carcinoma, serves as a clinically relevant model of this aggressive cancer. The adherent epithelial line retains key malignant features and is widely used in functional genomics and drug sensitivity studies, providing an appropriate background for investigating tumor suppressor gene function.
INHBE encodes inhibin subunit beta E, a TGF-?? superfamily ligand that activates ACVR2/ACVR1 receptor complexes, inducing phosphorylation of SMAD2/3. Phosphorylated SMAD2/3 partners with SMAD4 to regulate transcription of targets like p21 and apoptotic genes. Ligand activity is modulated by follistatin and relates to INHBA/INHBB-mediated signaling. This pathway controls cell proliferation, differentiation, and apoptosis through SMAD-dependent transcription.
In esophageal squamous cell carcinoma, INHBE likely exerts tumor-suppressive effects via SMAD-mediated growth inhibition and apoptosis. Knockout of INHBE in KYSE-150 cells eliminates this regulatory input, enabling dissection of TGF-??/activin signaling in tumor progression and potential roles in cancer cachexia. The model supports investigation of therapeutic vulnerabilities and mechanisms of resistance.
These polyclonal knockout cells are employed in proliferation, migration, and apoptosis assays to characterize phenotypic changes. Molecular profiling via western blotting and RT-qPCR assesses SMAD activation and target gene expression. Drug sensitivity testing facilitates identification of compounds with selective activity against INHBE-deficient esophageal cancer cells. For further information, please contact Ascent Research.
