CHI3L1 expression

This study found that the YKL-40 expression level was significantly stronger in low-grade than in high-grade canine cutaneous mast cell tumors and was associated with various clinical and pathological features. Stronger YKL-40 expression level correlated with longer survival time, especially in low-grade cMCTs. Therefore, YKL-40 could serve as a prognostic marker for cMCTs.

G721-0282 decreased N-cadherins and VCAM-1 in GBM spheroids, but the changes in the 2D model of U-87 MG glioblastoma cells were different; Inhibition of CHI3L1 has the potential to reduce the invasiveness of GBM tumors. The 3D model of GBM spheroids is of great significance for investigating changes in membrane proteins and the tumor microenvironment.

G721-0282 decreased N-cadherins and VCAM-1 in GBM spheroids, but the changes in the 2D model of U-87 MG glioblastoma cells were different; (4) Inhibition of CHI3L1 has the potential to reduce the invasiveness of GBM tumors. The proposed 3D model of GBM spheroids is of great significance for investigating changes in membrane proteins and the tumor microenvironment.

A bioinformatics analysis also identified a positive association between CHI3L1 expression and lymphangiogenesis or immunosuppression pathways. Our study established a clear association between stromal CHI3L1 expression and lymphatic metastasis, suggesting that stromal CHI3L1 expression is a potential prognostic marker for bladder cancer patients.

Lastly, the experimental results indicated that the alterations in IL18, SH2D2A, and CHI3L1 expression after treatment matched those in the public database. In this study, Five PTX-ICD-related biomarkers (CHI3L1, IL18, PAPLN, SH2D2A, and UBE2L6) were identified to aid in predicting BRCA treatment outcomes.

We present novel data for increased YKL-40 expression in tumor buds within the front of tumor invasion. We assume that the combination of this morphological parameter with the tissue level of the pleotropic YKL-40 glycoprotein could serve as a future prognostic biomarker for CRC stratification and treatment.

CHI3L1 gene expression serves as a robust molecular marker of connectivity and functionally influences TM networks. The connectivity signature allows insights into brain tumor biology, provides a proof-of-principle that tumor cell TM-connectivity is relevant for patients' prognosis, and serves as a robust prognostic biomarker.

The miR-375 inhibitor also significantly downregulated the IL-6, IL-1β, TNF-α, p-IκBα/IκBα, ROS, and NOX-4 expressions to alleviate oxidative stress and inflammation, which were reversed by the GPR39 inhibitor. An in vivo experiment proved that the miR-375 inhibitor upregulated the GPR39 expression and improved inflammation, oxidative stress, and endothelial cell damage associated with atherosclerosis.The miR-375 inhibitor improved inflammation, oxidative stress, and cell damage in ox-LDL-induced HAECs and HFD-induced ApoE mice by promoting the GPR39 expression, which provided a new theoretical basis for the clinical treatment of atherosclerosis.

Together, these data reveal that pSTAT3+ RA-derived CHI3L1 is associated with BrM invasion, implicating STAT3 and CHI3L1 as clinically relevant therapeutic targets for the treatment of HI BrM.

Overall, by knockdown of the COG3 gene, MT1-MMP and YKL40 were dropped, leading to suppressed angiogenesis along with decreasing migration and proliferation. SiRNA-COG3 may be an ideal agent to consider for clinical trial assessment therapy for OC, especially when an antiangiogenic SNAR-pathway targeting drug.

In patients with locally advanced GC after curative resection, expression of the CHI3L1 in GC tissue may be a useful prognostic marker.

Mechanistically, Chi3l1 promoted neutrophil recruitment and neutrophil extracellular trap formation, which blocked T cell infiltration. Our findings provide insight into the mechanism underlying stromal restriction of CD8 T cells and suggest that targeting Chi3l1 may promote anti-tumor immunity in various tumor types.

Furthermore, this article also provides a brief overview of the various mechanisms and inhibitors employed to inhibit CHI3L1 and disrupt its interaction with receptors. These endeavors highlight the pivotal roles of CHI3L1 and suggest therapeutic approaches targeting CHI3L1 in the development of metabolic diseases, neurodegenerative diseases, and cancers.

Elevated CHI3L1 expression was associated with genes which were related to the recruitment and infiltration of neutrophils. Consequently, CHI3L1 may serve as a novel evaluation factor for the degree of neutrophil infiltration in advanced bladder cancer in those scheduled for chemotherapy.

Pharmacological blocking of CHI3L1 with an antibody reduced TM networks, thus providing a handle for future clinical translation. Together, these data identify a functional and upstream role of CHI3L1 in governing tumor cell connectivity, CHI3L1 RNA and protein expression as a novel way to determine overall GBC connectivity for future trials, and finally a new therapeutic target for tumor network-disrupting strategies.

We used the TCGA and CGGA databases to analyze the effect of EMP3 and CHI3L1 expression on the prognosis of glioma patients and their correlation with gene expression using bioinformation analysis. The results showed that low-grade glioma patients with a low expression of EMP3 and CHI3L1 had a better prognosis, and EMP3 and CHI3L1 co-expression genes were correlated. The combination of these two factors could be a new prognostic index for glioma patients.

Interestingly, higher CHI3L1 expression levels were found to be associated with longer progression-free survival rates in PCa patients. Our findings indicated that levels of CHI3L1 may influence the progression of PCa, and the rs6691378 and 10399805 SNP genetic variants of CHI3L1 are linked to the clinicopathological development of PCa within a Taiwanese population.

YKL-40 can promote the expression and secretion of IL-6, IL-8, and other acute inflammatory factors in A549 cell line, a type Ⅱ alveolar epithelial cell model, thus aggravating the inflammatory response. Targeted inhibition of YKL-40 expression may effectively inhibit inflammatory response.

Circ_TNFRSF21 plays a significant role in cSCC progression by enhancing cell proliferation, migration, invasion, and M2 macrophage polarization through inhibiting miR-214-3p and subsequent disinhibition of CHI3L1. These findings deepen our understanding of the molecular mechanism of cSCC and propose the circ_TNFRSF21/miR-214-3p/CHI3L1 axis as promising diagnosis markers or therapeutic targets for cSCC.

YKL-40 might participate in MF pathophysiology, and the highest expression is associated with advanced stages of the disease and poor outcomes. Therefore, it might be of value as a prognosticator for monitoring high-risk MF patients and follow-up assessment of treatment success.

Inhibiting CHI3L1 and disrupting its interaction with its receptors through multiple mechanisms of action are briefly discussed. These endeavors highlight the pivotal roles of astrocytic CHI3L1 in neurological disorders and could contribute to the development of effective inhibitors based on the strategy of structure-based drug discovery, which could be an attractive therapeutic approach for neurological disease treatment.

The expression of YKL-40 was significantly higher in CRC tumor tissue compared to healthy tissue and correlated with MMP-8, IL17A, and PD-L1 expression. In silico analysis revealed an association of YKL-40 with disease recurrence, and GSEA revealed a potential link between elevated YKL-40 expression and immunosuppressive properties of the tumor microenvironment in CRC.

Six independent cohorts of CRC patients were stratified by YKL-40 tissue expression to define its prognostic role and its effect on cetuximab and oxaliplatin treatment response. YKL-40 high-expressing HCT116 and Caco2 cells showed increased motility, invasion and proliferation. Our study recognizes a novel role of YKL-40 tissue expression in promoting CRC metastatic potential, through EMT signaling activation, and provides significant clinical implications that may impact the risk prediction of patients with mCRC. YKL-40 high tissue levels also strengthen a predictive value for better cetuximab responsiveness, even in patients with KRAS mutations. Since resistance to cetuximab remains one of the greatest challenges in treating CRC, our findings may be crucial for developing novel YKL-40-targeted therapy approaches.

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.

Neoadjuvant toripalimab plus chemotherapy was safe and effective, with a high MPR and manageable TRAEs for II-III NSCLC, even converting initially PRD to RD. Disparate transcriptomic characteristics of therapeutic efficiency were observed, and CHI3L1 expression predicted therapeutic response and survival.

CHI3L1 was highly expressed in acute appendicitis and appendiceal mucinous neoplasms, which can be used as a novel biomarker predicting appendicitis.

Strikingly, high YKL-40 tissue levels showed a predictive value for a better response to cetuximab, even in patients with stage IV CRC and mutant KRAS, and worse sensitivity to oxaliplatin. Taken together, our findings establish that tissue YKL-40 overexpression enhances CRC metastatic potential, highlighting this gene as a novel prognostic candidate, a predictive biomarker for therapy response, and an attractive target for future therapy in CRC.

The expression level of serum CHI3L1 was significantly higher in patients with liver fibrosis than that in patients without liver fibrosis. The expression levels of serum CHI3L1 were different in different grades of liver fibrosis and increased with the severity of liver fibrosis. Serum CHI3L1 can distinguish early stage (S1) of liver fibrosis from late stage (S3-4) of liver fibrosis. Serum CHI3L1 combined with HA is even more effective in the diagnosis of S2-4 hepatic fibrosis. The diagnostic efficacy of serum CHI3L1 in patients with ALT ≤ 2ULN was better than that of the other non-invasive diagnostic models.

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. 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.

Lu-177-DTPA-YKL40 antibodies significantly inhibited tumor growth in ovarian cancer xenograft mice. Our study indicated that In-111/Lu-177-DTPA-YKL40 neutralizing antibodies could be potential companion theranostic agents for patients with EOC.

In addition, CHI3L1 also correlated with immune cell infiltration and immune checkpoints. Our study suggests that inhibition of CHI3L1 may help to reduce immunosuppression and overcome immunotherapy resistance, which would be an therapeutic area for the treatment of GBM.

Its high expression can promote neovascularization in the tumor microenvironment. CHI3L1 is a potential therapeutic target in the context of cervical cancer.

The observed effect of COS could be due to the blocking of YKL-40-receptor binding inhibiting cancer-promoting signaling pathways. Alternative biological functions of COS could also be involved.

Combining the serum CHI3L1 and α-fetoprotein (AFP) by a binary logistic regression model can increase the diagnostic sensitivity to 97.5%. Multivariate Cox regression analysis indicated that CHI3L1 is an independent prognostic factor in patients with HCC.

Overall, our findings shed light on the important link between tumor associated bacteria and CHI3L1 in cancer progression. Identifying the mechanism of action through which microbiota and CHI3L1 influence cancer growth will open new possibilities for improved screening, prognosis, and survival for patients with breast cancer.

This blocking of the CHI3L1-IL-13Rα2 signal caused the inhibition of c-Jun N-terminal kinase (JNK)-activator protein-1 (AP-1) signals, resulting in the prevention of lung metastasis and cancer cell growth. Our data demonstrate that K284 may serve as a potential candidate anti-cancer compound targeting CHI3L1.

CHI3L1 overexpression may favor macrophage recruitment in esophageal tumor tissues. Future studies are needed to delineate the mechanisms of CHI3L1-mediated macrophage recruitment and polarization in tumor tissues.

GPR39 was upregulated in colon cancer tissues compared with tumor-adjacent tissues. GPR39 was an independent prognostic biomarker in colon cancer for poor prognosis. EPCAM and PD-L1 were substantially associated with GPR39 expression, and they were also identified as prognostic biomarkers in colon cancers.