ArticleCellular and molecular gastroenterology and hepatology2026
Opposing Effects of LRIG1 and LRIG3 on EGFR Maintain Intestinal Homeostasis and Mitigate Likelihood of Colonic Neoplasia.
Article in Cellular and molecular gastroenterology and hepatology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
BACKGROUND &
aimsEpidermal growth factor receptor signaling maintains intestinal homeostasis by modulating proliferation and differentiation within the stem cell compartment, with excess epidermal growth factor receptor (EGFR) signaling predisposing to neoplasia. EGFR protein levels are central to EGFR function. These levels are negatively regulated by leucine-rich repeats and immunoglobulin-like domains 1 (LRIG1), which accelerates receptor internalization and degradation, supporting a tumor suppressor role for LRIG1. Leucine-rich repeats and immunoglobulin-like domains 3 (LRIG3) is a less-studied family member that has been reported, in a context-dependent manner, to both cooperate with and oppose the effects of LRIG1 on epidermal growth factor receptor.
methodsTo examine the function of LRIG3 relative to LRIG1 on EGFR levels and downstream signaling in vivo, we generated an Lrig3 floxed allele and intercrossed these mice with Lrig1
resultsUnlike the heightened EGFR and Wnt activity caused by Lrig1 loss, loss of Lrig3 in Lrig1
conclusionsThese findings indicate that LRIG3 and LRIG1 oppose one another to balance EGFR signaling, maintain intestinal homeostasis, and minimize the likelihood of colonic neoplasia.
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