Journal: International Journal of Chronic Obstructive Pulmonary Disease

Article Title: LAMC2 Drives Airway Remodeling in COPD via EMT Regulation Through the AKT Pathway

doi: 10.2147/COPD.S580964

Figure Lengend Snippet: Airway remodeling and LAMC2 upregulation are observed in both COPD patients and mouse models. ( A ) Representative Masson’s trichrome-stained lung sections from non-smokers (n=5), smokers without COPD (n=5), and COPD patients (n=5). Scale bar: 250μm. ( B ) Quantitative staining of Masson content in non-smoker (n=5), smoker (n=5), and COPD (n=5). ( C ) Representative Masson’s trichrome staining of lung sections from air-exposed control mice (n=5) and COPD model mice (n=5). Scale bar: 100μm. ( D ) Quantitative staining of Masson content in air-control (n=5) and COPD model mice (n=5). ( E ) LAMC2 expression levels in airway epithelial cells from non-smokers (n=12), smokers (n=12), and COPD patients (n=6) based on the GSE5058 dataset. ( F ) Representative airway LAMC2 immunohistochemical staining on lung sections of non-smoker (n=5), smoker (n=5), and COPD (n=5). Scale bar: 50μm. ( G ) Quantitative staining of LAMC2 intensity on airway epithelium of non-smoker (n=5), smoker (n=5), and COPD (n=5). ( H ) LAMC2 expression levels in lung tissues from air-control (n=30) and COPD model mice (n=34) based on the GSE87292 dataset. ( I ) Western blot and ( J ) quantitative analysis of LAMC2 protein expression in the lung tissue from mice from different groups (n=3 mice/group). ( K ) Representative airway LAMC2 immunohistochemical staining on lung sections of air-control (n=5) and COPD model mice (n=5).Scale bar: 100μm. ( L ) Quantitative staining of LAMC2 intensity on airway epithelium of air-control (n=5) and COPD model mice (n=5). Data presented as the means ± SD. * P < 0.05, ** P < 0.01.

Article Snippet: The membranes were blocked with 5% bovine serum albumin for 1 hour at room temperature and then incubated overnight at 4°C with the following primary antibodies: GAPDH (1:5000; Cell Signaling Technology, Danvers, MA, USA), LAMC2 (1:1000; Proteintech, China), E-Cadherin (1:1000; Cell Signaling Technology), N-Cadherin (1:1000; Cell Signaling Technology), Fibronectin (1:1000; HUABIO, China), AKT (1:1000; Cell Signaling Technology), and phospho-AKT (p-AKT, 1:1000; Cell Signaling Technology).

Techniques: Staining, Control, Expressing, Immunohistochemical staining, Western Blot

Journal: International Journal of Chronic Obstructive Pulmonary Disease

Article Title: LAMC2 Drives Airway Remodeling in COPD via EMT Regulation Through the AKT Pathway

doi: 10.2147/COPD.S580964

Figure Lengend Snippet: Knockdown of LAMC2 attenuates airway remodeling and EMT in a COPD model. ( A ) Schematic overview of the animal experimental design and grouping. ( B ) Representative Masson staining on mice lung sections from different groups (n = 5 per group). ( C ) Quantitative staining of Masson content in different groups (n = 5 per group). ( D ) Representative airway Fibronectin immunohistochemical staining and ( E ) quantitative staining of Fibronectin intensity on lung sections of different groups (n = 5 per group). ( F ) Representative airway N-cadherin immunohistochemical staining and ( G ) quantitative staining of N-cadherin intensity on lung sections of different groups (n=5 per group). ( H ) Representative airway E-cadherin immunohistochemical staining and ( I ) quantitative staining of E-cadherin intensity on lung sections of different groups (n=5 per group). ( J – M ) Western blot analysis and quantification of EMT-related proteins (Fibronectin, N-cadherin, and E-cadherin) in lung tissues from the different treatment groups. * P < 0.05, ** P < 0.01, *** P < 0.001. Scale bars: 100μm.

Article Snippet: The membranes were blocked with 5% bovine serum albumin for 1 hour at room temperature and then incubated overnight at 4°C with the following primary antibodies: GAPDH (1:5000; Cell Signaling Technology, Danvers, MA, USA), LAMC2 (1:1000; Proteintech, China), E-Cadherin (1:1000; Cell Signaling Technology), N-Cadherin (1:1000; Cell Signaling Technology), Fibronectin (1:1000; HUABIO, China), AKT (1:1000; Cell Signaling Technology), and phospho-AKT (p-AKT, 1:1000; Cell Signaling Technology).

Techniques: Knockdown, Staining, Immunohistochemical staining, Western Blot

Journal: International Journal of Chronic Obstructive Pulmonary Disease

Article Title: LAMC2 Drives Airway Remodeling in COPD via EMT Regulation Through the AKT Pathway

doi: 10.2147/COPD.S580964

Figure Lengend Snippet: LAMC2 expression is upregulated in bronchial epithelial cells following TGF-β1 stimulation. ( A and B ) Volcano plots illustrating DEGs from ( A ) GSE104908 and ( B ) GSE40374 datasets, with corresponding LAMC2 expression levels. Significantly upregulated genes (red) and downregulated genes (blue) are indicated (fold change >1.5, adjusted P < 0.05). ( C ) The mRNA levels of Fibronectin, N-cadherin, E-cadherin, and LAMC2 after treatment with different concentrations of TGF-β1 for 24 hours. ( D ) Western blot and ( E – H ) the relative protein level of Fibronectin, N-cadherin, E-cadherin, and LAMC2 after treatment with different concentrations of TGF-β1 for 24 hours. The data are the mean ± SD. * P < 0.05, ** P < 0.01, *** P < 0.001.

Article Snippet: The membranes were blocked with 5% bovine serum albumin for 1 hour at room temperature and then incubated overnight at 4°C with the following primary antibodies: GAPDH (1:5000; Cell Signaling Technology, Danvers, MA, USA), LAMC2 (1:1000; Proteintech, China), E-Cadherin (1:1000; Cell Signaling Technology), N-Cadherin (1:1000; Cell Signaling Technology), Fibronectin (1:1000; HUABIO, China), AKT (1:1000; Cell Signaling Technology), and phospho-AKT (p-AKT, 1:1000; Cell Signaling Technology).

Techniques: Expressing, Western Blot

Journal: International Journal of Chronic Obstructive Pulmonary Disease

Article Title: LAMC2 Drives Airway Remodeling in COPD via EMT Regulation Through the AKT Pathway

doi: 10.2147/COPD.S580964

Figure Lengend Snippet: Knockdown of LAMC2 reverses TGF-β1-induced EMT marker expression and inhibits 16HBE cell migration. ( A ) LAMC2 mRNA expression levels following transfection with different siLAMC2 constructs. ( B ) mRNA expression of Fibronectin, N-cadherin, and E-cadherin after siLAMC2 transfection and subsequent TGF-β1 treatment. ( C ) Western blot and ( D – F ) the relative protein level of Fibronectin, N-cadherin, E-cadherin, and LAMC2 after siLAMC2 transfection and TGF-β1 treatment. ( G ) Representative images of wound healing and transwell migration assays under different treatment conditions. Scale bar: 20 μm. ( H ) Quantification of migration rate (%) from wound healing assay and ( I ) Cell migration numbers counted from transwell assays. The data are the mean ± SD. ** P < 0.01, *** P < 0.001.

Article Snippet: The membranes were blocked with 5% bovine serum albumin for 1 hour at room temperature and then incubated overnight at 4°C with the following primary antibodies: GAPDH (1:5000; Cell Signaling Technology, Danvers, MA, USA), LAMC2 (1:1000; Proteintech, China), E-Cadherin (1:1000; Cell Signaling Technology), N-Cadherin (1:1000; Cell Signaling Technology), Fibronectin (1:1000; HUABIO, China), AKT (1:1000; Cell Signaling Technology), and phospho-AKT (p-AKT, 1:1000; Cell Signaling Technology).

Techniques: Knockdown, Marker, Expressing, Migration, Transfection, Construct, Western Blot, Wound Healing Assay

Journal: International Journal of Chronic Obstructive Pulmonary Disease

Article Title: LAMC2 Drives Airway Remodeling in COPD via EMT Regulation Through the AKT Pathway

doi: 10.2147/COPD.S580964

Figure Lengend Snippet: Overexpression of LAMC2 promotes TGF-β1-induced EMT and enhances 16HBE cell migration. ( A ) LAMC2 mRNA expression levels following transfection with LAMC2 plasmid and TGF-β1treatment. ( B ) mRNA expression of Fibronectin, N-cadherin, and E-cadherin after LAMC2 plasmid vector transfection and subsequent TGF-β1 treatment. ( C ) Western blot and ( D – F ) the relative protein level of Fibronectin, N-cadherin, E-cadherin, and LAMC2 after LAMC2 plasmid vector transfection and TGF-β1 treatment. ( G ) Representative images of wound healing and transwell migration assays under different treatment conditions. Scale bar: 20 μm. ( H ) Quantification of migration rate (%) from wound healing assay and ( I ) Cell migration numbers counted from transwell assays. The data are the mean ± SD. * P < 0.05, ** P < 0.01, *** P < 0.001.

Article Snippet: The membranes were blocked with 5% bovine serum albumin for 1 hour at room temperature and then incubated overnight at 4°C with the following primary antibodies: GAPDH (1:5000; Cell Signaling Technology, Danvers, MA, USA), LAMC2 (1:1000; Proteintech, China), E-Cadherin (1:1000; Cell Signaling Technology), N-Cadherin (1:1000; Cell Signaling Technology), Fibronectin (1:1000; HUABIO, China), AKT (1:1000; Cell Signaling Technology), and phospho-AKT (p-AKT, 1:1000; Cell Signaling Technology).

Techniques: Over Expression, Migration, Expressing, Transfection, Plasmid Preparation, Western Blot, Wound Healing Assay

Journal: International Journal of Chronic Obstructive Pulmonary Disease

Article Title: LAMC2 Drives Airway Remodeling in COPD via EMT Regulation Through the AKT Pathway

doi: 10.2147/COPD.S580964

Figure Lengend Snippet: LAMC2 facilitates EMT in 16HBE cells through activation of the AKT signaling pathway. ( A ) GO enrichment analysis of down-regulated DEGs from RNA-seq data, showing the top three most significantly enriched terms in each category: Biological Process (BP), Cellular Component (CC), and Molecular Function (MF) (adjusted P < 0.05). Terms are ranked by gene count. ( B ) KEGG pathway analysis of down-regulated DEGs. Statistically significant pathways (adjusted P < 0.05) are visualized in a dot plot. ( C ) Western Blot and ( D ) Immunofluorescence detection, and ( E – G ) the relative protein level of AKT and p-AKT after si-NC/LAMC2 transfection and TGF-β1 treatment. ( H ) Western Blot and ( I ) Immunofluorescence detection, and ( J – L ) the relative protein level of AKT and p-AKT after LAMC2 plasmid vector transfection and TGF-β1 treatment. Scale bar: 50 μm. The data are the mean ± SD. * P < 0.05, ** P < 0.01, *** P < 0.001.

Article Snippet: The membranes were blocked with 5% bovine serum albumin for 1 hour at room temperature and then incubated overnight at 4°C with the following primary antibodies: GAPDH (1:5000; Cell Signaling Technology, Danvers, MA, USA), LAMC2 (1:1000; Proteintech, China), E-Cadherin (1:1000; Cell Signaling Technology), N-Cadherin (1:1000; Cell Signaling Technology), Fibronectin (1:1000; HUABIO, China), AKT (1:1000; Cell Signaling Technology), and phospho-AKT (p-AKT, 1:1000; Cell Signaling Technology).

Techniques: Activation Assay, RNA Sequencing, Western Blot, Immunofluorescence, Transfection, Plasmid Preparation

Journal: bioRxiv

Article Title: Cell-of-Origin, not Oncogenic Effect, Determines Desmoplastic Immune Exclusion in KRAS-Driven Liver Cancer

doi: 10.64898/2026.03.24.711280

Figure Lengend Snippet: Multi-omics integration identifies LAMC2, uPA and BSSP-4 as CCA-specific secreted factors. (A) Schematic of the experimental workflow to collect material for secretome and proteome analysis. (B) Venn diagram showing the overlap of PK-induced transcriptional and secretory responses in chol-orgs. Intersections include PK-upregulated genes in chol-orgs from RNA-seq (chol-PK vs chol-WT, bottom-left), PK-upregulated proteins in chol-orgs from secretome (CCM, bottom-right), genes whose PK-induced expression is stronger in interaction effects (interaction contrast, upper-right), and proteins predicted to be secreted according to the Human Protein Atlas (upper-left). (C) Bubble plot showing cross-dataset support for candidate PK-associated genes identified by the integrative analysis in (B). Rows indicate 15 selected genes from (B), and columns indicate the indicated in-house murine result and public human datasets. Dot color encodes z-scored log2 FC (z(LFC). Filled circles indicate significant differences (padj < 0.1) and open circles indicate non-significant results. Dot size reflects statistical strength-log10(padj).

Article Snippet: The antibodies used in this study were: Lamc2 (Proteintech, #19698-1-AP), uPA (Proteintech, #17968-1-AP), BSSP4 (ThermoFisher Scientific, #PA5-47245), and rabbit-IgG (Millipore, #pp64).

Techniques: Biomarker Discovery, RNA Sequencing, Expressing

Journal: bioRxiv

Article Title: Cell-of-Origin, not Oncogenic Effect, Determines Desmoplastic Immune Exclusion in KRAS-Driven Liver Cancer

doi: 10.64898/2026.03.24.711280

Figure Lengend Snippet: LAMC2 and uPA affect HSC activation and impair CCA formation in vivo . (A) Schematic overview of the in vitro fibroblast activation assay, where murine HSCs were treated with CCM from chol-PK and neutralizing antibodies. (B) Scatter plot indicating mRNA expression of Acta2 and Col1a1 in mHSCs treated with Chol-PK CCM and indicated neutralizing antibodies or control IgG. (n=5 from 2 independent experiments). (C) Schematic of scratch assay with mHSCs treated with low FBS (2%) media supplemented with respective recombinant protein. (D) Plot depicting mean relative wound coverage upon scratch injury over time with indicated recombinant protein at different dosage (n≥17 from 3 experiments). (E) Schematic of in vivo validation model: Chol-PK organoids were edited by CRISPR/Cas9 to generate Prss22 -, Lamc2 -, or Plau -deleted lines, which were orthotopically implanted into the liver and harvested at the same time point. (F) Macroscopic images of liver tumors 7 weeks after implantation of indicated lines. (G) Bar plot with respective tumor penetrance per line. (H) Representative histopathology images of liver tumors obtained upon orthotopic implantation of chol-PK and indicated KO lines. Stains as indicated. Red dotted line demarcates the boundary between non-tumor liver (N) and tumor (T). All scale bars are 100 μm. (I) Scatter plot depicting the total CD3 + and CD8 + T cell density per area per tumor for the indicated lines.

Article Snippet: The antibodies used in this study were: Lamc2 (Proteintech, #19698-1-AP), uPA (Proteintech, #17968-1-AP), BSSP4 (ThermoFisher Scientific, #PA5-47245), and rabbit-IgG (Millipore, #pp64).

Techniques: Activation Assay, In Vivo, In Vitro, Expressing, Control, Wound Healing Assay, Recombinant, Biomarker Discovery, CRISPR, Histopathology