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BackgroundCanopy FGF signalling regulator 3 (CNPY3) is involved in immune regulation, tumorigenesis and development, nevertheless, its role in glioma remains largely unexplored. Our study aimed to explore the regulatory role of CNPY3 as a prognostic biomarker in human glioma cell migration, invasion and immune infiltration.MethodsBioinformatics analysis of CNPY3 and clinical relevance of glioma in public databases was performed. COX regression analysis was performed to assess the relationship between CNPY3 and glioma prognosis. GO and Kyoto Encyclopedia of Genes and Genomes analyses were conducted to predict the signaling pathways of CNPY3 in gliomas. Tumor immune infiltration was explored using TIMER, CIBERSORT, and Pearson correlation analysis. GSVA analysis and single-cell sequencing data were employed for further validation. The effects of CNPY3 on the migration and invasion of glioma cells were investigated through cell scratch assay and transwell assay.ResultsCNPY3 was positively correlated with IDH mutation status, 1p/19q status, histopathologic grade, and MGMT promoter methylation status, but negatively with the overall survival of glioma patients (< 0.05). CNPY3 was significantly associated with tumor immune response, inflammatory response, and lipopolysaccharide-mediated signaling pathway. CNPY3 influenced different types of immune cells which affected the immune microenvironment of glioma. CNPY3 promoted the increase of M2 macrophage and was negatively correlated with the positive regulation of macrophages apoptotic process. In vitro data suggested the promotion of CNPY3 in U87MG cells was associated with an increased capacity for cell migration and invasion (< 0.05). Tumor drug sensitivity analysis showed more sensitivity towards temozolomide, irinotecan, and cisplatin among high CNPY3 expression patients (< 0.05).ConclusionIncreased CNPY3 expression impacts the immune microenvironment of glioma and enhances the migration and invasion of glioma. CNPY3 is recommended as a prognostic biomarker for glioma patients.
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http://dx.doi.org/10.1177/18758592251328162 | DOI Listing |
Cancer Metastasis Rev
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Institute for Integrative Biology of the Cell (I2BC), Université Paris-Saclay, CEA, CNRS, Gif-Sur-Yvette, 91198, France.
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State Key Laboratory of Metabolic Dysregulation & Prevention and Treatment of Esophageal Cancer, Tianjian Laboratory of Advanced Biomedical Sciences, Department of Radiology, Department of Clinical Research and Translational Medicine, The Third Affiliated Hospital of Zhengzhou University, Zhengzhou,
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School of Life Sciences, Anhui Medical University, Hefei, 230032, China; Translational Research Institute of Henan Provincial People's Hospital, Henan International Joint Laboratory of Non-coding RNA and Metabolism in Cancer, Henan Provincial Key Laboratory of Long Non-coding RNA and Cancer Metaboli
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Department of Thoracic Surgery, Affiliated Hospital of Zunyi Medical University, 149 Dalian Road, Zunyi, 563000, Guizhou, China; The Public Experimental Center of Medicine, Affiliated Hospital of Zunyi Medical University, 149 Dalian Road, Zunyi, 563000, Guizhou, China. Electronic address: kexixian@z
Chemotherapy resistance in lung adenocarcinoma (LUAD) limits clinical efficacy. In this study, we first established circ_IGF2BP1 knockdown models in LUAD cells (A549 and H1299). Using dual-luciferase reporter assays, functional analyses, and miR-885-3p rescue experiments, we demonstrated that circ_IGF2BP1 promotes LUAD cell proliferation, migration, and invasion by directly targeting miR-885-3p.
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Department of Pathology, The Second Affiliated Hospital of Anhui Medical University, Hefei, Anhui 230601, PR China; Department of Pathology, The First Affiliated Hospital of Anhui Medical University, Hefei, Anhui 230061, PR China. Electronic address:
Tumor-associated neutrophils (TANs) play a critical role in breast cancer progression. This study demonstrated that high CD66b TANs infiltration correlated with poor disease-free survival (DFS) and promoted proliferation, migration, and invasion of breast cancer cells in vitro. Conversely, the immune-related long non-coding RNA C6orf99 was downregulated in breast cancer and associated with favorable DFS.
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