DLL3 regulates Notch signaling in small cell lung cancer

Jun W Kim
Stanford University
January 1, 2022
iScience
https://pubmed.ncbi.nlm.nih.gov/36483011

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

https://pubmed.ncbi.nlm.nih.gov/36483011

Research summary

This study investigates the role of Delta-like ligand 3 (DLL3) in modulating Notch signaling in small cell lung cancer (SCLC). Using a mouse model with Rosa26-targeted, inducible DLL3 expression, researchers showed that DLL3 suppresses Notch signaling, alters tumor cell fate, and increases intratumoral heterogeneity. The model enabled precise analysis of DLL3’s contribution to neuroendocrine differentiation and its potential as a therapeutic target.

Key outcome of the study

Inducible DLL3 expression suppresses Notch signaling, reshapes tumor differentiation, and enhances heterogeneity in SCLC; DLL3 is validated as a regulator and therapeutic target.

Model

Rosa26 Knockin mouse model with Cre-inducible expression of DLL3 using IRES technology, allowing bicistronic expression with a reporter.

TARGET:
Dll3
Delta-like ligand 3

Keywords

Small cell lung cancer, Notch signaling, Tumor heterogeneity, Neuroendocrine tumors

Technical specifications

Rosa26 Knockin, IRES-reporter, Inducible expression, DLL3, Cre-lox

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