ArticleMolecules (Basel, Switzerland)2022
A Natural CHI3L1-Targeting Compound, Ebractenoid F, Inhibits Lung Cancer Cell Growth and Migration and Induces Apoptosis by Blocking CHI3L1/AKT Signals.
Article in Molecules (Basel, Switzerland), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 18 citations in OpenAlex.
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- CHI3L1 promotes cell division through activation of RhoA in lung cancer cells.Cell communication and signaling : CCS · 2025Article
- Neuroinflammatory Mechanisms and Therapeutic Targets in Oxaliplatin-Induced Peripheral Neuropathy: a Comprehensive Review.Neurotoxicity research · 2025Review
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- Human chitinases and chitinase-like proteins as emerging drug targets - a medicinal chemistry perspective.RSC medicinal chemistry · 2025Review
- Anti-CHI3L1 antibody suppresses colon cancer growth through downregulation of VEGFA and NAMPT expression.Archives of pharmacal research · 2025Article
- The role of Wnt/β-catenin signaling in lung cancer progression and therapy: a comprehensive review.Medical oncology (Northwood, London, England) · 2025Review
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- Significance of chitinase-3-like protein 1 in the pathogenesis of inflammatory diseases and cancer.Experimental & molecular medicine · 2024Review
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Authors and funding
13 authors at 2 institutions in 1 country.
Funding
Abstract
Our previous big data analyses reported a strong association between CHI3L1 expression and lung tumor development. In this present study, we investigated whether a CHI3L1-inhibiting natural compound, ebractenoid F, inhibits lung cancer cell growth and migration and induces apoptosis. Ebractenoid F concentration-dependently (0, 17, 35, 70 µM) and significantly inhibited the proliferation and migration of A549 and H460 lung cancer cells and induced apoptosis. In the mechanism study, we found that ebractenoid F bound to CHI3L1 and suppressed CHI3L1-associated AKT signaling. Combined treatment with an AKT inhibitor, LY294002, and ebractenoid F synergistically decreased the expression of CHI3L1. Moreover, the combination treatment further inhibited the growth and migration of lung cancer cells and further induced apoptosis, as well as the expression levels of apoptosis-related proteins. Thus, our data demonstrate that ebractenoid F may serve as a potential anti-lung cancer compound targeting CHI3L1-associated AKT signaling.
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