Anti‐Chi3L1 antibody suppresses lung tumor growth and metastasis through inhibition of M2 polarization

Yu, Ji Eun; Yeo, In Jun; Son, Dong Ju; Yun, Jaesuk; Han, Sang‐Bae; Hong, Jin Tae

doi:10.1002/1878-0261.13152

Cited by 22 publications

(15 citation statements)

References 63 publications

(94 reference statements)

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“…For instance, the inhibitory effects of chitinase 3-like 1 on lung cancer are associated with STAT6-dependent M2 polarization inhibition. 55 A recent study found that targeting the Th2-STAT6-C3-NET (neutrophil extracellular trap) signalling axis effectively inhibited breast cancer metastasis to the lungs. 56 Another study reported that p53 mutations may promote malignancy in solitary fibrous tumours by regulating the NAB2-STAT6 fusion gene at the transcriptional level.…”

Section: Discussionmentioning

confidence: 99%

Potential role of PRKCSH in lung cancer: bioinformatics analysis and a case study of Nano ZnO

et al. 2022

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Section: Discussionmentioning

confidence: 99%

Potential role of PRKCSH in lung cancer: bioinformatics analysis and a case study of Nano ZnO

et al. 2022

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“…Blotting. Cell lysis and western blotting were performed as previously described [54]. Cells were lysed with lysis bufer (20 mM Tris-HCl pH 7.8, 0.1% NP-40, 200 mM NaCl, 2 mM EDTA, 5 mM EGTA with protease inhibitor, and protease inhibitor) and centrifuged at 13,000 × g for 20 min at 4 °C.…”

Section: Cell Lysates Preparation and Westernmentioning

confidence: 99%

“…Te RT-qPCR assay was performed as previously described [54]. Total RNA was isolated using RiboEx Total RNA ( # 301-001, GeneAll Biotechnology Co., Seoul, Korea) and reverse transcribed into cDNA using the High-Capacity cDNA Reverse Transcription Kit ( # 4368813, Applied Biosystems, Foster City, CA), according to the manufacturer's protocol.…”

Section: Rt-qpcr Assaymentioning

confidence: 99%

Bee Venom Triggers Autophagy-Induced Apoptosis in Human Lung Cancer Cells via the mTOR Signaling Pathway

Kim

Hong

et al. 2022

Journal of Oncology

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In oriental medicine, bee venom has long been used as a therapeutic agent against inflammatory diseases. Several studies have reported that isolated and purified bee venom components are effective in treating dementia, arthritis, inflammation, bacterial infections, and cancer. In previous studies, we reported that bee venom inhibits cell growth and induces apoptotic cell death in lung cancer cells. In the present study, we assessed whether bee venom affects autophagy and thereby induces apoptosis. Bee venom treatment increased the levels of autophagy-related proteins (Atg5, Beclin-1, and LC3-II) and the accumulation of LC3 puncta. We found that bee venom could induce autophagy by inhibiting the mTOR signaling pathway. In addition, we found that hydroxychloroquine (HCQ)- or si-ATG5-induced autophagy inhibition further demoted bee venom-induced apoptosis. Bee venom-induced autophagy promotes apoptosis in lung cancer cells and may become a new approach to cancer treatment.

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“…Chitinase-3-like protein 1 (CHI3L1), a member of the glycoside hydrolase family 18 13 , plays crucial roles in oxidative injury, apoptosis, pyroptosis, extracellular matrix regulation, Th1/Th2 inflammatory balance, and parenchymal scarring 14 . Non-enzymatic CHI3L1 is highly expressed in various cancer types, such as lung 15 , colon, gastric, and breast cancers 16 , and is associated with low survival rates of patients with cancer. In particular, up-regulated CHI3L1 and CD44 are considered as markers of mesenchymal (MES) glioma 17 that predominantly manifested NF-κB activation 18 .…”

Section: Introductionmentioning

confidence: 99%

Chitinase-3 like-protein-1 promotes glioma progression via the NF-κB signaling pathway and tumor microenvironment reprogramming

Zhao¹,

Zeng²,

Xu³

et al. 2022

Theranostics

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Background: Chitinase-3-like protein 1 (CHI3L1) is overexpressed in various types of tumors, especially in glioma, and contributes to tumor progression. However, the definite role of CHI3L1 and involved pathway in glioma progression are not completely understood. Methods: CHI3L1 expression in human gliomas and its association with patient survival was determined using enzyme-linked immunosorbent assay, western blot, immunohistochemistry, and public databases. Single-cell RNA-seq was used to characterize the landscape of tumor and myeloid cells. Human proteome microarray assay was applied to identify the binding partners of CHI3L1. Protein-protein interactions were analyzed by co-immunoprecipitation and cellular co-localization. The roles of CHI3L1 in glioma proliferation and invasion were investigated in tumor cell lines by gain- and loss- of function, as well as in vivo animal experiments. Results: CHI3L1 was up-regulated in all disease stages of glioma, which was closely related with tumor survival, growth, and invasion. CHI3L1 was primarily expressed in glioma cells, followed by neutrophils. Moreover, glioma cells with high expression of CHI3L1 were significantly enriched in NF-κB pathway. Pseudo-time trajectory analysis revealed a gradual transition from CHI3L1 low to CHI3L1 high glioma cells, along with the NF-κB pathway gradually reversed from inhibition to activation. Intriguingly, CHI3L1 binds to actinin alpha 4 (ACTN4) and NFKB1, and enhances the NF-κB signaling pathway by promoting the NF-κB subunit nuclear translocation in glioma cells. Further, CHI3L1 were released into the tumor microenvironment (TME) and interacted with CD44 expressed on tumor-associated macrophages to activate AKT pathway, thereby contributing to M2 macrophage polarization. In addition, CHI3L1 positively correlated to the expression of immune checkpoints, such as CD274 (PD-L1) and HAVCR2 (LAG3), which then remodeled the TME to an immunosuppressive phenotype. Conclusion: Our research revealed that CHI3L1 facilitated NF-κB pathway activation within glioma cells and reprogramed the TME, thereby serving as a promising therapeutic target for glioma.

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Anti‐Chi3L1 antibody suppresses lung tumor growth and metastasis through inhibition of M2 polarization

Cited by 22 publications

References 63 publications

Potential role of PRKCSH in lung cancer: bioinformatics analysis and a case study of Nano ZnO

Potential role of PRKCSH in lung cancer: bioinformatics analysis and a case study of Nano ZnO

Bee Venom Triggers Autophagy-Induced Apoptosis in Human Lung Cancer Cells via the mTOR Signaling Pathway

Chitinase-3 like-protein-1 promotes glioma progression via the NF-κB signaling pathway and tumor microenvironment reprogramming

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