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Published on: July 21, 2018
CRABP2 Promotes Lung Adenocarcinoma Through Retinoic Acid Pathway-Mediated NF-κB Activation
XiRui Zhu1, BiaoFeng Fan1, Qing Lei1
1Department of Thoracic Surgery II, The Third Affiliated Hospital of Kunming Medical University, Yunnan Cancer Hospital, Yunnan Cancer Center, 650118 Kunming, Yunnan, China.
Frontiers in Bioscience (Landmark Edition)
|July 30, 2026
Summary
Cellular retinoic acid-binding protein 2 (CRABP2) drives lung adenocarcinoma (LUAD) progression by activating the nuclear factor kappa B (NF-κB) pathway. Targeting this CRABP2/RA/NF-κB axis offers a potential therapeutic strategy for LUAD treatment.
Area of Science:
- Oncology
- Molecular Biology
- Cancer Research
Background:
- Lung adenocarcinoma (LUAD) is a leading cause of cancer mortality.
- Tumor heterogeneity and resistance limit current targeted therapies for LUAD.
- Identifying novel oncogenic drivers is crucial for improving LUAD treatment outcomes.
Purpose of the Study:
- To identify novel oncogenic drivers in LUAD.
- To elucidate the underlying mechanisms of LUAD progression.
- To explore potential therapeutic targets for LUAD.
Main Methods:
- Assessed cellular retinoic acid-binding protein 2 (CRABP2) expression in LUAD specimens.
- Performed in vitro (proliferation, migration, invasion, apoptosis) and in vivo xenograft assays.
- Utilized RNA sequencing, KEGG pathway analysis, and immunoblotting to investigate the NF-κB signaling pathway.
Main Results:
- CRABP2 acts as an oncogene in LUAD, promoting tumor growth, migration, and invasion while inhibiting apoptosis.
- CRABP2 activates the nuclear factor kappa B (NF-κB) pathway via retinoic acid (RA) signaling.
- CRABP2-induced NF-κB activation is RA-dependent and mediates oncogenic effects.
Conclusions:
- Established a CRABP2/RA/NF-κB signaling axis driving LUAD progression.
- This pathway represents a potential therapeutic target for LUAD intervention.
- Findings provide insights into LUAD pathogenesis and treatment strategies.
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