ArticleTheranostics2023
Induction of ER stress-mediated apoptosis through SOD1 upregulation by deficiency of CHI3L1 inhibits lung metastasis.
Article in Theranostics, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 20 citations in OpenAlex.
- SRPRA affects hyperoxia-induced bronchopulmonary dysplasia by modulating endoplasmic reticulum stress through the CHOP pathway.Journal of cardiothoracic surgery · 2026Article
- CHI3L1: a novel regulator of vascular remodeling in pulmonary arterial hypertension.Molecular and cellular biochemistry · 2026Article
- Integrative analysis of Poly(A)-seq and RNA-seq reveals transcriptional regulation of poly(A) tail length in tuberculosis.Microbiology spectrum · 2026Article
- PABPC1-induced stabilization of PGK1 mRNA reduces apoptosis and sunitinib sensitivity in renal cell carcinoma by suppressing endoplasmic reticulum stress.Cell death & disease · 2026Article
- CHI3L1 is a diagnostic biomarker involved in immune infiltration of gastric cancer.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026Article
- CHI3L1 Is Associated With TP53 Signaling and Promotes Papillary Thyroid Carcinoma Progression.Cancer reports (Hoboken, N.J.) · 2026Article
- Lactylated chitinase-3-like protein 1 promotes the development of sepsis.Central-European journal of immunology · 2026Article
- CHI3L1 promotes cell division through activation of RhoA in lung cancer cells.Cell communication and signaling : CCS · 2025Article
- Safflower Polysaccharides Alleviate TNBS-Induced Colitis by Modulating Gut Immunity.Foods (Basel, Switzerland) · 2025Article
- Cancer cell-derived migrasomes harboring ATF6 promote breast cancer brain metastasisCancer biology & medicine · 2025Article
- TRAF3IP3 Induces ER Stress-Mediated Apoptosis with Protective Autophagy to Inhibit Lung Adenocarcinoma Proliferation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- RETRACTION: Bee Venom Triggers Autophagy-Induced Apoptosis in Human Lung Cancer Cells via the mTOR Signaling Pathway.Journal of oncology · 2025Article
- Article
- Identification and validation of protein biomarkers for predicting gastrointestinal stromal tumor recurrence.Computational and structural biotechnology journal · 2024Article
- HCP5 Derived Novel Microprotein Triggers Progression of Gastric Cancer through Regulating Ferroptosis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- The cGAS-STING/PERK-eIF2α: Individual or Potentially Collaborative Signaling Transduction in Cardiovascular Diseases.International journal of biological sciences · 2024Review
Corrections and comments
- Erratum issued
Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chitinase-3-like protein 1 (CHI3L1), which is secreted by immune and inflammatory cells, is associated with several inflammatory diseases. However, the basic cellular pathophysiological functions of CHI3L1 are not well characterized. To investigate the novel pathophysiological function of CHI3L1, we performed LC-MS/MS analysis of cells transfected with Myc-vector and Myc-CHI3L1. We analyzed the changes in the protein distribution in Myc-CHI3L1 transfected-cells, and identified 451 differentially expressed proteins (DEPs) compared with Myc-vector-transfected-cells. The biological function of the 451 DEPs was analyzed and it was found that the proteins with endoplasmic reticulum (ER)-associated function were much more highly expressed in CHI3L1-overexpressing cells. We then compared and analyzed the effect of CHI3L1 on the ER chaperon levels in normal lung cells and cancer cells. We identified that CHI3L1 is localized in the ER. In normal cells, the depletion of CHI3L1 did not induce ER stress. However, the depletion of CHI3L1 induces ER stress and eventually activates the unfolded protein response, especially the activation of Protein kinase R-like endoplasmic reticulum kinase (PERK), which regulates protein synthesis in cancer cells. CHI3L1 may not affect ER stress owing to the lack of misfolded proteins in normal cells, but instead activate ER stress as a defense mechanism only in cancer cells. Under ER stress conditions induced by the application of thapsigargin, the depletion of CHI3L1 induces ER stress through the upregulation of PERK and PERK downstream factors (eIF2α and ATF4) in both normal and cancer cells. However, these signaling activations occur more often in cancer cells than in normal cells. The expression of Grp78 and PERK in the tissues of patients with lung cancer was higher compared with healthy tissues. It is well known that ER stress-mediated PERK-eIF2α-ATF4 signaling activation causes apoptotic cell death. ER stress-mediated apoptosis induced by the depletion of CHI3L1 occurs in cancer cells, but rarely occurs in normal cells. Consistent with results from the
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