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VLA-Precision: Asymmetric Co-Bootstrapping for Efficient Real-World Online RL of Vision-Language-Action Models
Transmembrane glycoprotein BSG serves a dual role as a prognostic and immunological modulator in the tumor microenvironment of lung adenocarcinoma
Transl Oncol. 2026 Sep 8;73:102990. doi: 10.1016/j.tranon.2026.102990. Online ahead of print.
ABSTRACT
BACKGROUND: Lung adenocarcinoma (LUAD) is a predominant and lethal subtype of non-small cell lung cancer, with a lack of reliable prognostic biomarkers to guide clinical management. Basigin (BSG) has been implicated in tumor progression across multiple cancers, yet its expression pattern, prognostic significance, and underlying mechanisms in LUAD remain incompletely elucidated.
METHODS: We integrated multi-omics data from TCGA, GTEx, CCLE, and GEO databases to analyze BSG expression profiles. Clinical correlations were assessed via Kruskal-Wallis tests. Prognostic value was determined using Kaplan-Meier survival analysis, univariate/multivariate Cox regression, and nomogram construction with calibration curves. Functional enrichment (GO/KEGG) and immune infiltration analyses were performed to explore BSG-related mechanisms, followed by immunohistochemical (IHC) validation in A549 cells and clinical LUAD tissue microarrays.
RESULTS: BSG was significantly upregulated in LUAD tissues versus normal/paired adjacent tissues, correlating with advanced T/N/pathologic stages. High BSG expression predicted worse survival outcomes in TCGA-LUAD, which was validated in GEO datasets. Multivariate Cox regression identified BSG as an independent prognostic factor, with a well-calibrated nomogram for survival prediction. Functional exploration indicated that BSG mainly participated in tumor-associated and immunological pathways. Immune infiltration analysis indicated that BSG was significantly correlated with the infiltration of various immune cells. Moreover, BSG exhibited a strong association with immune checkpoint proteins, chemokines, chemokine receptors, and MHC genes. IHC further confirmed its cytoplasmic/membranous localization and prognostic relevance.
CONCLUSION: BSG serves as an independent prognostic biomarker and potential therapeutic target in LUAD, shedding light on its regulatory roles in tumor progression and immune microenvironment remodeling.
PMID:42710246 | DOI:10.1016/j.tranon.2026.102990
Transmembrane glycoprotein BSG serves a dual role as a prognostic and immunological modulator in the tumor microenvironment of lung adenocarcinoma
Transl Oncol. 2026 Sep 8;73:102990. doi: 10.1016/j.tranon.2026.102990. Online ahead of print.
ABSTRACT
BACKGROUND: Lung adenocarcinoma (LUAD) is a predominant and lethal subtype of non-small cell lung cancer, with a lack of reliable prognostic biomarkers to guide clinical management. Basigin (BSG) has been implicated in tumor progression across multiple cancers, yet its expression pattern, prognostic significance, and underlying mechanisms in LUAD remain incompletely elucidated.
METHODS: We integrated multi-omics data from TCGA, GTEx, CCLE, and GEO databases to analyze BSG expression profiles. Clinical correlations were assessed via Kruskal-Wallis tests. Prognostic value was determined using Kaplan-Meier survival analysis, univariate/multivariate Cox regression, and nomogram construction with calibration curves. Functional enrichment (GO/KEGG) and immune infiltration analyses were performed to explore BSG-related mechanisms, followed by immunohistochemical (IHC) validation in A549 cells and clinical LUAD tissue microarrays.
RESULTS: BSG was significantly upregulated in LUAD tissues versus normal/paired adjacent tissues, correlating with advanced T/N/pathologic stages. High BSG expression predicted worse survival outcomes in TCGA-LUAD, which was validated in GEO datasets. Multivariate Cox regression identified BSG as an independent prognostic factor, with a well-calibrated nomogram for survival prediction. Functional exploration indicated that BSG mainly participated in tumor-associated and immunological pathways. Immune infiltration analysis indicated that BSG was significantly correlated with the infiltration of various immune cells. Moreover, BSG exhibited a strong association with immune checkpoint proteins, chemokines, chemokine receptors, and MHC genes. IHC further confirmed its cytoplasmic/membranous localization and prognostic relevance.
CONCLUSION: BSG serves as an independent prognostic biomarker and potential therapeutic target in LUAD, shedding light on its regulatory roles in tumor progression and immune microenvironment remodeling.
PMID:42710246 | DOI:10.1016/j.tranon.2026.102990
LC-ERD: Mining Latent Logic for Self-Evolving Reasoning via Consistency-Regulated Reward Decomposition
SMDD-Bench: Can LLMs Solve Real-World Small Molecule Drug Design Tasks?
Correction: Steroid receptor coactivator-1 facilitates METTL3-mediated m6A modification by coactivating NF-κB and promotes the malignant progression of glioblastoma
Oncogene, Published online: 15 April 2026; doi:10.1038/s41388-026-03788-8
Correction: Steroid receptor coactivator-1 facilitates METTL3-mediated m6A modification by coactivating NF-κB and promotes the malignant progression of glioblastomaBeyond Matching to Tiles: Bridging Unaligned Aerial and Satellite Views for Vision-Only UAV Navigation
Integrated Multi-Omics Analysis Reveals Modulation of the Ras Pathway by Siji Kangbingdu Mixture in Acute Lung Injury
Comb Chem High Throughput Screen. 2026 Mar 11. doi: 10.2174/0113862073398293251205055042. Online ahead of print.
ABSTRACT
INTRODUCTION: This study aimed to investigate the protective effects of Siji Kangbingdu Mixture (SKM) against acute lung injury (ALI) in mice and to elucidate its underlying mechanisms.
METHODS: ALI was induced in Kunming mice via intranasal administration of LPS (5 mg/kg), followed by oral SKM treatment for 7 days. Lung wet-to-dry (W/D) ratio, histopathology, multiomics analysis, and network pharmacology were performed. Key targets and pathways were identified through dynamic KEGG analysis and validated by Western blotting.
RESULTS: SKM treatment ameliorated alveolar hemorrhage, alveolar wall disruption, septal thickening, edema, and inflammatory cell infiltration. Integrated multi-omics analysis revealed that SKM primarily modulated the Ras signaling pathway, reducing the protein expression of Phospho- MEK1/2, Raf1, Phospho-ERK1/2, and RASH/RASK/RASN, thereby contributing to the treatment of ALI.
DISCUSSION: SKM alleviated LPS-induced ALI in mice by inhibiting the Ras pathway, highlighting the pathway's role in ALI pathogenesis. However, due to limitations of the animal model and incomplete validation, further studies combining clinical research and in vitro experiments are needed to confirm its efficacy and mechanism.
CONCLUSIONS: SKM shows potential to ameliorate ALI by suppressing inflammatory responses and reducing local tissue fibrosis. The combination of metabolomics, transcriptomics, and network pharmacology elucidated its mechanism, while Western blot analysis suggested that its therapeutic effect is associated with downregulation of the Ras signaling pathway.
PMID:41830142 | DOI:10.2174/0113862073398293251205055042
Integrated Multi-Omics Analysis Reveals Modulation of the Ras Pathway by Siji Kangbingdu Mixture in Acute Lung Injury
Comb Chem High Throughput Screen. 2026 Mar 11. doi: 10.2174/0113862073398293251205055042. Online ahead of print.
ABSTRACT
INTRODUCTION: This study aimed to investigate the protective effects of Siji Kangbingdu Mixture (SKM) against acute lung injury (ALI) in mice and to elucidate its underlying mechanisms.
METHODS: ALI was induced in Kunming mice via intranasal administration of LPS (5 mg/kg), followed by oral SKM treatment for 7 days. Lung wet-to-dry (W/D) ratio, histopathology, multiomics analysis, and network pharmacology were performed. Key targets and pathways were identified through dynamic KEGG analysis and validated by Western blotting.
RESULTS: SKM treatment ameliorated alveolar hemorrhage, alveolar wall disruption, septal thickening, edema, and inflammatory cell infiltration. Integrated multi-omics analysis revealed that SKM primarily modulated the Ras signaling pathway, reducing the protein expression of Phospho- MEK1/2, Raf1, Phospho-ERK1/2, and RASH/RASK/RASN, thereby contributing to the treatment of ALI.
DISCUSSION: SKM alleviated LPS-induced ALI in mice by inhibiting the Ras pathway, highlighting the pathway's role in ALI pathogenesis. However, due to limitations of the animal model and incomplete validation, further studies combining clinical research and in vitro experiments are needed to confirm its efficacy and mechanism.
CONCLUSIONS: SKM shows potential to ameliorate ALI by suppressing inflammatory responses and reducing local tissue fibrosis. The combination of metabolomics, transcriptomics, and network pharmacology elucidated its mechanism, while Western blot analysis suggested that its therapeutic effect is associated with downregulation of the Ras signaling pathway.
PMID:41830142 | DOI:10.2174/0113862073398293251205055042