The GPNMB Knockout LoVo Polyclonal Cells product consists of a CRISPR/Cas9-edited polyclonal knockout cell population targeting the GPNMB gene in LoVo human colorectal adenocarcinoma cells. This heterogeneous pool, generated by Cas9-mediated disruption of the GPNMB locus, avoids clonal selection artifacts and preserves genetic diversity, making it suitable for functional genomic screens, signaling studies, and pooled assays. The loss-of-function model enables robust investigation of GPNMB-dependent processes without the limitations of single-cell clones.
LoVo cells originate from a metastatic colon adenocarcinoma and harbor well-characterized oncogenic mutations in KRAS, APC, and TP53. As an epithelial colorectal cancer model, LoVo recapitulates driver mutations prevalent in advanced colorectal tumors and is widely employed to study metastasis, drug resistance, and tumor?Cmicroenvironment interactions. The cell line’s genetic background provides a disease-relevant context for examining oncogenic signaling networks and invasive behavior.
GPNMB is a type I transmembrane glycoprotein that interacts with integrins ??5??1 and ??V??3, leading to FAK and Src phosphorylation. Downstream ERK1/2 signaling upregulates MMP-2 and MMP-9, promoting invasion. Expression is induced by TGF-??, HIF1A, and STAT3, and GPNMB associates with CD44, integrating microenvironmental signals to enhance cell migration and immune evasion. Collectively, GPNMB enhances integrin-mediated outside-in signaling, facilitating tumor cell migration and metastatic dissemination.
In the LoVo background, which is driven by KRAS activation and p53 deficiency, GPNMB likely cooperates with oncogenic pathways to sustain an invasive phenotype. Disruption of GPNMB is expected to impair FAK/Src/ERK/MMP signaling, reducing migratory and invasive capacity. The polyclonal knockout population mirrors intratumoral heterogeneity, allowing researchers to quantify functional consequences of GPNMB loss in a diverse cell pool. This model is particularly valuable for studying colorectal cancer metastasis, enabling direct assessment of how GPNMB loss alters integrin-dependent adhesion, matrix degradation, and signaling dynamics.
This product supports Boyden chamber migration/invasion assays, western blotting for phospho-FAK and phospho-ERK, RT-qPCR for GPNMB mRNA, and flow cytometry for integrins. Co-immunoprecipitation can probe GPNMB?Cintegrin interactions, and in vivo models assess metastasis. The cells enable high-content screening, functional rescue, and studies of TGF-??/HIF1A/STAT3-mediated regulation. For further information or custom modifications, please contact Ascent Research.
