Journal: Functional & Integrative Genomics

Article Title: A clinically relevant SLC2A1-associated malignant epithelial cell state predicts prognosis and immunotherapy response in lung adenocarcinoma

doi: 10.1007/s10142-026-01897-x

Figure Lengend Snippet: Causal inference and functional prediction of SLC2A1 in LUAD. ( A ) Mendelian randomization (MR) analysis assessing the causal effect of SLC2A1 on lung adenocarcinoma (LUAD). ( B ) Leave-one-out sensitivity analysis evaluating the influence of individual SNPs on the MR estimates for SLC2A1 and LUAD. ( C ) Causal effect estimates of SLC2A1 obtained using different MR methods (IVW and MR-Egger). ( D ) Scatter plot showing the relationships between SNP effects on SLC2A1 and LUAD risk. ( E ) UMAP visualization of SLC2A1 expression in single-cell transcriptomic data. ( F ) Proportion of SLC2A1-positive cells across different cell types. ( G ) Comparison of SLC2A1 expression levels in epithelial cells between normal and LUAD samples. ( H ) Ranking of differentially regulated genes following virtual knockout of SLC2A1. ( I ) Distribution of network Z-scores in the virtual knockout analysis. ( J ) Hallmark pathways affected by virtual knockout of SLC2A1. ( K ) Hallmark gene set enrichment analysis (GSEA) based on genes associated with virtual knockout of SLC2A1

Article Snippet: The membranes were incubated with primary antibodies against SLC2A1 (1:1000; A6982, ABclonal) and GAPDH (1:5000; ab128915, Abcam), followed by incubation with appropriate secondary antibodies.

Techniques: Functional Assay, Expressing, Single Cell, Comparison, Knock-Out

Journal: Functional & Integrative Genomics

Article Title: A clinically relevant SLC2A1-associated malignant epithelial cell state predicts prognosis and immunotherapy response in lung adenocarcinoma

doi: 10.1007/s10142-026-01897-x

Figure Lengend Snippet: Expression patterns and clinical relevance of SLC2A1 in LUAD. ( A ) Comparison of SLC2A1 mRNA expression between normal lung tissues and lung adenocarcinoma (LUAD) tissues in the TCGA cohort. ( B ) Kaplan–Meier overall survival (OS) curves stratified by SLC2A1 expression levels. ( C ) Kaplan–Meier progression-free survival (PFS) curves stratified by SLC2A1 expression levels. ( D ) Representative immunohistochemistry (IHC) images of SLC2A1 protein in normal lung and LUAD tissues. ( E ) Comparison of SLC2A1 protein IHC scores between normal lung and LUAD tissues. ( F ) Correlation analysis between SLC2A1 copy number alterations and its mRNA expression. ( G ) Distribution of SLC2A1 expression across different copy number alteration groups (shallow deletion, diploid, gain, and amplification). ( H ) Heatmap showing the relationship between SLC2A1 expression levels and common gene mutation profiles. ( I ) Comparison of SLC2A1 expression levels according to TP53 and TTN mutation status

Article Snippet: The membranes were incubated with primary antibodies against SLC2A1 (1:1000; A6982, ABclonal) and GAPDH (1:5000; ab128915, Abcam), followed by incubation with appropriate secondary antibodies.

Techniques: Expressing, Comparison, Immunohistochemistry, Amplification, Mutagenesis

Journal: Functional & Integrative Genomics

Article Title: A clinically relevant SLC2A1-associated malignant epithelial cell state predicts prognosis and immunotherapy response in lung adenocarcinoma

doi: 10.1007/s10142-026-01897-x

Figure Lengend Snippet: SLC2A1 promotes proliferation, migration, and invasion of LUAD cells. ( A ) Relative mRNA expression levels of SLC2A1 in LUAD cell lines (A549, PC9, H1299, H1975) and normal bronchial epithelial cells (BEAS-2B) measured by qRT-PCR. ( B ) Protein expression levels of SLC2A1 in the indicated cell lines determined by Western blotting. ( C , D ) Knockdown efficiency of SLC2A1 in A549 and H1975 cells validated by qRT-PCR ( C ) and Western blotting ( D ) after siRNA transfection. ( E ) Cell proliferation assessed by CCK-8 assay in A549 and H1975 cells following SLC2A1 silencing. ( F , G ) Wound-healing assays showing reduced migration ability in SLC2A1-knockdown cells compared with control cells. ( H , I ) Transwell assays demonstrating decreased migration and invasion capacities in A549 and H1975 cells after SLC2A1 knockdown. Data are presented as mean ± SD from three independent experiments. * P < 0.05, ** P < 0.01, *** P < 0.001

Article Snippet: The membranes were incubated with primary antibodies against SLC2A1 (1:1000; A6982, ABclonal) and GAPDH (1:5000; ab128915, Abcam), followed by incubation with appropriate secondary antibodies.

Techniques: Migration, Expressing, Quantitative RT-PCR, Western Blot, Knockdown, Transfection, CCK-8 Assay, Control

Journal: Functional & Integrative Genomics

Article Title: A clinically relevant SLC2A1-associated malignant epithelial cell state predicts prognosis and immunotherapy response in lung adenocarcinoma

doi: 10.1007/s10142-026-01897-x

Figure Lengend Snippet: Interaction between SLC2A1-positive epithelial cells and CAFs in LUAD. ( A , B ) Network diagrams showing intercellular interactions among different cell types in tumor samples. A ) number of interactions; B ) interaction strength. ( C ) Heatmap of outgoing signaling patterns across different cell types. ( D ) Heatmap of incoming signaling patterns across different cell types. ( E ) Analysis of differential signaling pathways transmitted from fibroblasts to SLC2A1-positive and SLC2A1-negative epithelial cells. ( F ) Intercellular communication network of the COLLAGEN signaling pathway. ( G ) COLLAGEN–receptor interaction pairs transmitted from fibroblasts to SLC2A1-positive and SLC2A1-negative epithelial cells. ( H ) Expression distribution of COLLAGEN-related genes across different cell types. ( I ) UMAP visualization of fibroblast subpopulations. ( J ) Network diagram showing interaction strength between fibroblast subpopulations and SLC2A1-positive/negative epithelial cells. ( K ) Heatmap of interaction strength between different fibroblast subpopulations and epithelial cells. ( L ) Communication strength between fibroblast subpopulations and SLC2A1-positive epithelial cells. ( M ) Comparison of COLLAGEN signaling pathway communication strength among different fibroblast subpopulations

Article Snippet: The membranes were incubated with primary antibodies against SLC2A1 (1:1000; A6982, ABclonal) and GAPDH (1:5000; ab128915, Abcam), followed by incubation with appropriate secondary antibodies.

Techniques: Protein-Protein interactions, Expressing, Comparison

Journal: Cancer Management and Research

Article Title: Hyperbaric Oxygen Reverses High-Glucose–Induced Stemness and Radioresistance in Non-Small Cell Lung Cancer Cells

doi: 10.2147/CMAR.S611017

Figure Lengend Snippet: High glucose increases Glut1 and HIF‑1α expression and stemness-associated markers in H1299 and A549 cells. H1299 and A549 cells were cultured in normal glucose (NG; 5.5 mM D-glucose) or high glucose (HG; 25 mM D-glucose) conditions and analyzed by Western blotting. Representative immunoblots show protein expression of Glut1, HIF‑1α, and the stemness-associated markers CD133, SOX2, and OCT4, with β-actin as the loading control. Bar graphs depict densitometric quantification of each target protein normalized to β-actin and expressed compared with that in the NG group. *P < 0.05 and **P < 0.01 versus the NG group.

Article Snippet: Membranes were blocked with bovine serum albumin (5%) and incubated with primary antibodies against Glut1 (1:1000; ABclonal; A6982; USA), HIF‐1α (1:1000; Proteintech; 20960-1-AP; USA), CD133 (1:500; Cell Signaling; #64326), SOX2 (1:500; 11,064-1-AP; Proteintech; USA), OCT4 (1:500; 11,263-1-AP; Proteintech; USA), and β-actin (1:20000; MAB1501R; Sigma-Aldrich; USA) overnight at 4°C.

Techniques: Expressing, Cell Culture, Western Blot, Control

Journal: Cancer Management and Research

Article Title: Hyperbaric Oxygen Reverses High-Glucose–Induced Stemness and Radioresistance in Non-Small Cell Lung Cancer Cells

doi: 10.2147/CMAR.S611017

Figure Lengend Snippet: Prolonged hyperbaric oxygen exposure suppresses HIF-1α and stemness-associated proteins in high-glucose-conditioned H1299 and A549 cells. H1299 and A549 cells maintained under high-glucose (HG; 25 mM D-glucose) conditions were exposed to hyperbaric oxygen (HBO) for 1 week (1w) or 4 weeks (4w). Protein expression of Glut1, HIF-1α, SOX2, and OCT4 was analyzed by Western blotting, with β-actin used as the loading control. Representative immunoblots are shown on the left, and bar graphs on the right and bottom panels show densitometric quantification of each target protein normalized to β-actin and expressed relative to the HG control without HBO (set to 1). Prolonged HBO exposure for 4 weeks significantly reduced HIF-1α, SOX2, and OCT4 expression in both H1299 and A549 cells, whereas Glut1 expression was not markedly altered. Asterisks indicate statistically significant differences compared with the HG control group in the corresponding cell line (**P < 0.01, ***P < 0.001).

Article Snippet: Membranes were blocked with bovine serum albumin (5%) and incubated with primary antibodies against Glut1 (1:1000; ABclonal; A6982; USA), HIF‐1α (1:1000; Proteintech; 20960-1-AP; USA), CD133 (1:500; Cell Signaling; #64326), SOX2 (1:500; 11,064-1-AP; Proteintech; USA), OCT4 (1:500; 11,263-1-AP; Proteintech; USA), and β-actin (1:20000; MAB1501R; Sigma-Aldrich; USA) overnight at 4°C.

Techniques: Expressing, Western Blot, Control