Description

The Chmp1b Knockout MC-38 Cell Line is a CRISPR/Cas9-edited knockout cell line featuring targeted disruption of the Chmp1b gene in MC-38 murine colon adenocarcinoma epithelial cells. This model enables loss-of-function studies of CHMP1B, a component of the ESCRT-III complex, to dissect its roles in membrane scission, multivesicular body formation, and cytokinesis within a colorectal cancer context.

MC-38 cells originate from a C57BL/6 mouse colorectal adenocarcinoma and serve as a widely used syngeneic tumor model for immunology and oncology research. These epithelial cells retain key tumor characteristics, making them ideal for investigating colorectal cancer biology, tumor-host interactions, and immune responses in an immunocompetent microenvironment.

CHMP1B is a core ESCRT-III subunit that mediates membrane scission in processes such as endosomal sorting and cytokinetic abscission. Its activity is regulated by cellular stress and growth factor signaling, and it forms functional complexes with CHMP2A, CHMP4B, VPS4 ATPase, and IST1. Downstream, CHMP1B governs EGFR degradation, Notch signaling, and autophagic flux. Thus, Chmp1b knockout disrupts endosomal trafficking, altering receptor turnover and membrane dynamics that impact cell proliferation and homeostasis.

In the context of MC-38 colorectal cancer cells, loss of Chmp1b impairs ESCRT-III-dependent pathways critical for oncogenic signaling. Sustained EGFR activity due to reduced degradation, along with dysregulated Notch and autophagy, can influence tumor cell survival, migration, and metastasis. This knockout model provides a platform to study how membrane trafficking defects reshape tumor cell behavior and the tumor microenvironment, offering insights into colorectal cancer progression.

Research applications include ESCRT biology, endosomal trafficking, cancer signaling, and tumor microenvironment studies. The cell line supports biochemical assays (western blotting, immunofluorescence, flow cytometry) and functional analyses (EGFR degradation assay, cytokinesis assessment, migration assay). By enabling precise genetic dissection in a syngeneic model, it facilitates investigation of CHMP1B-dependent mechanisms in colorectal cancer. For additional information or technical support, please contact Ascent Research.