NEDD9 Overexpression Causes Hyperproliferation of Luminal Cells and Cooperates with HER2 Oncogene in Tumor Initiation: A Novel Prognostic Marker in Breast Cancer

January 1, 2023
Cancers (Basel)
https://pubmed.ncbi.nlm.nih.gov/36831460

This article is currently being updated. View its version on PubMed.

https://pubmed.ncbi.nlm.nih.gov/36831460

Research summary

This study investigates the role of NEDD9 overexpression in mammary gland development and its cooperation with the HER2 oncogene in tumor initiation. The researchers generated a conditional transgenic mouse model with NEDD9 overexpression targeted to the Rosa26 locus. When crossed with MMTV-Cre mice, NEDD9 overexpression led to mammary epithelial hyperplasia, increased branching, and expansion of luminal epithelial cells. Co-expression with the Erbb2 (neu) oncogene accelerated the development of preneoplastic lesions.

Key outcome of the study

NEDD9 overexpression in the mammary gland induces hyperplasia and expansion of luminal epithelial cells. When combined with Erbb2 overexpression, it accelerates tumor initiation, suggesting that NEDD9 acts as a facilitator of HER2-driven tumorigenesis and may serve as a prognostic marker in breast cancer.

Mouse model

NEDD9 conditional overexpression mouse model developed by genOway, featuring a cDNA sequence for human NEDD9 under the control of the CAG promoter, inserted into the Rosa26 locus with a floxed STOP cassette, allowing for tissue-specific expression upon Cre recombination.

TARGET:
Nedd9
Neural precursor cell expressed, developmentally downregulated 9; HEF1; Cas-L

Keywords

Breast cancer, HER2-positive tumors, Mammary gland development, Tumor initiation, Prognostic biomarkers

Technical specifications

Conditional overexpression model, Rosa26 locus targeting, CAG promoter, Floxed STOP cassette, MMTV-Cre driver, HER2/Erbb2 cooperation

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Quick KI mouse

The Rosa26 and Hprt gene loci are well suited for gene over-expression, reduced development time and cost with ready-to-use targeting vectors.