ArticleScientific reports2023
CHI3L1 induces autophagy through the JNK pathway in lung cancer cells.
Article in Scientific reports, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 13 citations in OpenAlex.
- Canonical lymphocyte chemokine receptors CXCR3 and CXCR5 modulate neuronal autophagy.Cell death and differentiation · 2026Article
- The CHI3L1 protein plays role as a protecting factor against autophagy in glioblastoma cells.Apoptosis : an international journal on programmed cell death · 2026Article
- Decoding autophagy in neuro-tumor crosstalk: from underlying mechanisms to translational opportunities.Theranostics · 2026Review
- Regulation of autophagy by oncogene DJ1 via the JNK signaling pathway in human ovarian cancer cells.Journal of ovarian research · 2025Article
- CHI3L1 promotes cell division through activation of RhoA in lung cancer cells.Cell communication and signaling : CCS · 2025Article
- RNA-binding proteins and autophagy in lung cancer: mechanistic insights and therapeutic perspectives.Discover oncology · 2025Review
- 4D marmoset brain map reveals MRI and molecular signatures for onset of multiple sclerosis-like lesions.Science (New York, N.Y.) · 2025Article
- Chitinase 3-like 1 overexpression aggravates hypoxia-reoxygenation injury in IEC-6 cells by inhibiting the PI3K/AKT signalling pathway.Experimental physiology · 2024Article
- IL-32γ Induced Autophagy Through Suppression of MET and mTOR Pathways in Liver Tumor Growth Inhibition.International journal of molecular sciences · 2024Article
- A 4D transcriptomic map for the evolution of multiple sclerosis-like lesions in the marmoset brain.bioRxiv : the preprint server for biology · 2023Article
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Authors and funding
8 authors at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
CHI3L1 is closely related to the molecular mechanisms of cancer cell migration, growth, and death. According to recent research, autophagy regulates tumor growth during various stages of cancer development. This study examined the association between CHI3L1 and autophagy in human lung cancer cells. In CHI3L1-overexpressing lung cancer cells, the expression of LC3, an autophagosome marker, and the accumulation of LC3 puncta increased. In contrast, CHI3L1 depletion in lung cancer cells decreased the formation of autophagosomes. Additionally, CHI3L1 overexpression promoted the formation of autophagosomes in various cancer cell lines: it also increased the co-localization of LC3 and the lysosome marker protein LAMP-1, indicating an increase in the production of autolysosomes. In mechanism study, CHI3L1 promotes autophagy via activation of JNK signaling. JNK may be crucial for CHI3L1-induced autophagy since pretreatment with the JNK inhibitor reduced the autophagic effect. Consistent with the in vitro model, the expression of autophagy-related proteins was downregulated in the tumor tissues of CHI3L1-knockout mice. Furthermore, the expression of autophagy-related proteins and CHI3L1 increased in lung cancer tissues compared with normal lung tissues. These findings show that CHI3L1-induced autophagy is triggered by JNK signals and that CHI3L1-induced autophagy could be a novel therapeutic approach to lung cancer.
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