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$RUNX2 increases the accumulation of MDA231 cells as micrometastases in bone marrow. (A) Experimental schedule for the bone colonization of MDA231‐derived cells in SCID mice. An osteogenic premetastatic niche (PMN) was established by injecting MDA231 CDH11 high <t>/ITGA5</t> high extracellular vesicles into SCID mice via the tail vein for 3 weeks (2 doses/week). MDA231 RUNX2‐OE cells and control cells were injected into the mice via the left ventricle. (B) H&E staining images demonstrating osteoblasts (indicated by red triangles) in homeostatic bone (HB) and the PMN. (C) X‐ray images showing the bone mass in the HB and the PMN microenvironments. (D) Bar charts quantifying the osteoblast number as the ratio of osteoblast counts to bone perimeter in /mm (N.Ob/B.Pm) and bone mass as the bone volume fraction (BV/TV). (E) Western blot analysis demonstrating increased RUNX2 protein levels in MDA231 RUNX2‐OE cells compared with those in control cells. (F) Representative X‐ray images, pan‐cytokeratin (pan‐CK) immunohistochemical staining images, and TRAP staining images showing osteolytic lesions, tumor cell distribution, and activated osteoclasts, respectively. (G) Pie charts depicting the incidence of DTCs, micrometastases (micromets), and osteolytic lesions formed by control cells and RUNX2‐OE cells within HB and the PMN. The scale bars in the inset images indicate 20 µm. (H) Bar charts quantifying the tumor surface, erosion surface, and the number of TRAP + osteoclasts normalized to the total bone surface (N.Oc/BS in mm 2 ). (I) Bar charts illustrating the abundance and size of micrometastases in the bone marrow of mice without detectable bone lesions. (J) Representative KI67 fluorescence immunohistochemical staining images. Pan‐CK was used to label the tumor cells, while DAPI was used to stain the nuclei. (K) Bar chart illustrating the reduced numbers of KI67 + tumor cells in micrometastases compared with tumor cells within bone colonization. The data are displayed as the means ± SDs. n.s., not significant; * p <0.05, ** p <0.01, *** p <0.001 compared with the corresponding controls, as determined by Student's t‐test.$
Itga5, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Images

1) Product Images from "The Osteoblastic Microenvironment Determines the Fate of Breast Cancer Cells Disseminated in the Bone Marrow"

Article Title: The Osteoblastic Microenvironment Determines the Fate of Breast Cancer Cells Disseminated in the Bone Marrow

Journal: Advanced Science

doi: 10.1002/advs.202509980

$RUNX2 increases the accumulation of MDA231 cells as micrometastases in bone marrow. (A) Experimental schedule for the bone colonization of MDA231‐derived cells in SCID mice. An osteogenic premetastatic niche (PMN) was established by injecting MDA231 CDH11 high /ITGA5 high extracellular vesicles into SCID mice via the tail vein for 3 weeks (2 doses/week). MDA231 RUNX2‐OE cells and control cells were injected into the mice via the left ventricle. (B) H&E staining images demonstrating osteoblasts (indicated by red triangles) in homeostatic bone (HB) and the PMN. (C) X‐ray images showing the bone mass in the HB and the PMN microenvironments. (D) Bar charts quantifying the osteoblast number as the ratio of osteoblast counts to bone perimeter in /mm (N.Ob/B.Pm) and bone mass as the bone volume fraction (BV/TV). (E) Western blot analysis demonstrating increased RUNX2 protein levels in MDA231 RUNX2‐OE cells compared with those in control cells. (F) Representative X‐ray images, pan‐cytokeratin (pan‐CK) immunohistochemical staining images, and TRAP staining images showing osteolytic lesions, tumor cell distribution, and activated osteoclasts, respectively. (G) Pie charts depicting the incidence of DTCs, micrometastases (micromets), and osteolytic lesions formed by control cells and RUNX2‐OE cells within HB and the PMN. The scale bars in the inset images indicate 20 µm. (H) Bar charts quantifying the tumor surface, erosion surface, and the number of TRAP + osteoclasts normalized to the total bone surface (N.Oc/BS in mm 2 ). (I) Bar charts illustrating the abundance and size of micrometastases in the bone marrow of mice without detectable bone lesions. (J) Representative KI67 fluorescence immunohistochemical staining images. Pan‐CK was used to label the tumor cells, while DAPI was used to stain the nuclei. (K) Bar chart illustrating the reduced numbers of KI67 + tumor cells in micrometastases compared with tumor cells within bone colonization. The data are displayed as the means ± SDs. n.s., not significant; * p <0.05, ** p <0.01, *** p <0.001 compared with the corresponding controls, as determined by Student's t‐test.$
Figure Legend Snippet: RUNX2 increases the accumulation of MDA231 cells as micrometastases in bone marrow. (A) Experimental schedule for the bone colonization of MDA231‐derived cells in SCID mice. An osteogenic premetastatic niche (PMN) was established by injecting MDA231 CDH11 high /ITGA5 high extracellular vesicles into SCID mice via the tail vein for 3 weeks (2 doses/week). MDA231 RUNX2‐OE cells and control cells were injected into the mice via the left ventricle. (B) H&E staining images demonstrating osteoblasts (indicated by red triangles) in homeostatic bone (HB) and the PMN. (C) X‐ray images showing the bone mass in the HB and the PMN microenvironments. (D) Bar charts quantifying the osteoblast number as the ratio of osteoblast counts to bone perimeter in /mm (N.Ob/B.Pm) and bone mass as the bone volume fraction (BV/TV). (E) Western blot analysis demonstrating increased RUNX2 protein levels in MDA231 RUNX2‐OE cells compared with those in control cells. (F) Representative X‐ray images, pan‐cytokeratin (pan‐CK) immunohistochemical staining images, and TRAP staining images showing osteolytic lesions, tumor cell distribution, and activated osteoclasts, respectively. (G) Pie charts depicting the incidence of DTCs, micrometastases (micromets), and osteolytic lesions formed by control cells and RUNX2‐OE cells within HB and the PMN. The scale bars in the inset images indicate 20 µm. (H) Bar charts quantifying the tumor surface, erosion surface, and the number of TRAP + osteoclasts normalized to the total bone surface (N.Oc/BS in mm 2 ). (I) Bar charts illustrating the abundance and size of micrometastases in the bone marrow of mice without detectable bone lesions. (J) Representative KI67 fluorescence immunohistochemical staining images. Pan‐CK was used to label the tumor cells, while DAPI was used to stain the nuclei. (K) Bar chart illustrating the reduced numbers of KI67 + tumor cells in micrometastases compared with tumor cells within bone colonization. The data are displayed as the means ± SDs. n.s., not significant; * p <0.05, ** p <0.01, *** p <0.001 compared with the corresponding controls, as determined by Student's t‐test.

Techniques Used: Derivative Assay, Control, Injection, Staining, Western Blot, Immunohistochemical staining, Fluorescence

The ITGA5 antagonist ATN‐161 reduces the incidence of bone colonization. (A–D) Experimental diagram (A), representative X‐ray, H&E staining, TRAP staining, and KI67 and pan‐CK immunofluorescence staining images (B), and bar charts demonstrating the inhibition of PTH‐reactivated bone colonization (C) and tumor surface normalized to the bone surface (D), in MDA231‐derived cells following ATN‐161 administration. (E–H) Experimental diagram (E), representative X‐ray, H&E staining, TRAP staining, and KI67 and pan‐CK immunofluorescence staining images (F), and bar charts displaying the blockade of E2‐supported bone colonization (G) and tumor surface normalized to the bone surface (H), in MCF7‐derived cells after ATN‐161 administration. The scale bars in the inset images indicate 20 µm. The data are presented as the means ± SDs. * p <0.05, ** p <0.01 compared with the respective control mice, as determined by Fisher's exact probability test or Student's t test.

Figure Legend Snippet: The ITGA5 antagonist ATN‐161 reduces the incidence of bone colonization. (A–D) Experimental diagram (A), representative X‐ray, H&E staining, TRAP staining, and KI67 and pan‐CK immunofluorescence staining images (B), and bar charts demonstrating the inhibition of PTH‐reactivated bone colonization (C) and tumor surface normalized to the bone surface (D), in MDA231‐derived cells following ATN‐161 administration. (E–H) Experimental diagram (E), representative X‐ray, H&E staining, TRAP staining, and KI67 and pan‐CK immunofluorescence staining images (F), and bar charts displaying the blockade of E2‐supported bone colonization (G) and tumor surface normalized to the bone surface (H), in MCF7‐derived cells after ATN‐161 administration. The scale bars in the inset images indicate 20 µm. The data are presented as the means ± SDs. * p <0.05, ** p <0.01 compared with the respective control mice, as determined by Fisher's exact probability test or Student's t test.

Techniques Used: Staining, Immunofluorescence, Inhibition, Derivative Assay, Control

CCK-8 Assay:

Article Title: O-GlcNAcylation of ITGA5 facilitates the occurrence and development of colorectal cancer.
Article Snippet: Accepted Manuscript O-GlcNAcylation of ITGA5 facilitates the occurrence and development of colorectal cancer Miao Yu, Songtao Chu, Bingyuan Fei, Xuedong Fang, Zhuo Liu PII: S0014-4827(19)30304-0 DOI: https://doi.org/10.1016/j.yexcr.2019.06.009 Reference: YEXCR 11464 To appear in: Experimental Cell Research Received Date: 9 May 2019 Revised Date: 6 June 2019 Accepted Date: 10 June 2019 Please cite this article as: M. Yu, S. Chu, B. Fei, X. Fang, Z. Liu, O-GlcNAcylation of ITGA5 facilitates the occurrence and development of colorectal cancer, Experimental Cell Research (2019), doi: https:// doi.org/10.1016/j.yexcr.2019.06.009.. This is a PDF file of an unedited manuscript that has been accepted for publication.. As a service to our customers we are providing this early version of the manuscript.

Image Search Results

Upregulated ITGA5 expression in the airways of asthma patients and in a TGF‐ β 1‐induced EMT model, and its association with impaired lung function. (A) ITGA5 expression in bronchial brushings from asthma patients compared with healthy volunteers ( GSE41862 ). (B) ITGA5 expression in sputum airway cells from patients with mild, moderate, and severe asthma ( GSE184433 ). (C) ITGA5 expression in bronchial brushing samples from moderate and severe asthma patients ( GSE76226 ). (D) ITGA5 expression in bronchial brushing samples from asthma patients ( GSE164015 ). (E) ITGA5 expression in airway mucosal samples from asthma patients and allergic non‐asthma controls ( GSE193816 ). (F) Differential distribution of ITGA5 in airway mucosal samples from asthma patients and allergic non‐asthma controls shown in a umap plot ( GSE193816 ). (G) ITGA5 expression in an in vitro TGF‐ β 1‐induced EMT model using human bronchial epithelial cells ( GSE40374 ). (H) Correlation heatmap between ITGA5 and mesenchymal markers (Fibronectin, N‐cadherin, Vimentin) and the epithelial marker E‐cadherin ( GSE40374 ). (I) Scatter plots depicting correlations between ITGA5 expression and sputum total leukocyte count, and lung function parameters: ΔFEV 1 , FEV 1 % predicted, FVC % predicted, and FEV 1 /FVC % predicted in asthma patients ( GSE184433 ). Data were presented as mean ± SEM. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001.

Journal: Cell Proliferation

Article Title: ITGA5 as a Dual Regulator of Epithelial‐Mesenchymal Transition and Epithelial Cell Anoikis Resistance: Functional Validation and Drug Prediction

doi: 10.1111/cpr.70190

Figure Lengend Snippet: Upregulated ITGA5 expression in the airways of asthma patients and in a TGF‐ β 1‐induced EMT model, and its association with impaired lung function. (A) ITGA5 expression in bronchial brushings from asthma patients compared with healthy volunteers ( GSE41862 ). (B) ITGA5 expression in sputum airway cells from patients with mild, moderate, and severe asthma ( GSE184433 ). (C) ITGA5 expression in bronchial brushing samples from moderate and severe asthma patients ( GSE76226 ). (D) ITGA5 expression in bronchial brushing samples from asthma patients ( GSE164015 ). (E) ITGA5 expression in airway mucosal samples from asthma patients and allergic non‐asthma controls ( GSE193816 ). (F) Differential distribution of ITGA5 in airway mucosal samples from asthma patients and allergic non‐asthma controls shown in a umap plot ( GSE193816 ). (G) ITGA5 expression in an in vitro TGF‐ β 1‐induced EMT model using human bronchial epithelial cells ( GSE40374 ). (H) Correlation heatmap between ITGA5 and mesenchymal markers (Fibronectin, N‐cadherin, Vimentin) and the epithelial marker E‐cadherin ( GSE40374 ). (I) Scatter plots depicting correlations between ITGA5 expression and sputum total leukocyte count, and lung function parameters: ΔFEV 1 , FEV 1 % predicted, FVC % predicted, and FEV 1 /FVC % predicted in asthma patients ( GSE184433 ). Data were presented as mean ± SEM. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001.

Article Snippet: ITGA5 (TargetMol, TMPJ‐00810) was covalently immobilised on a CM5 sensor chip (Cytiva, BR‐1005‐30) using the standard 1‐ethyl‐3‐(3‐dimethylaminopropyl) carbodiimide/N‐hydroxysuccinimide amine coupling chemistry.

Techniques: Expressing, In Vitro, Marker, Significance Assay

TGF‐ β 1 induced EMT and anoikis resistance in human bronchial epithelial cells (HBE135‐E6E7). (Aand B) Western blot analysis of EMT phenotype markers (ZO‐1, E‐cadherin, Occludin, Fibronectin, N‐cadherin, Vimentin) at 48 h and 72 h, respectively. (C and D) Protein expression level of ITGA5 in the TGF‐ β 1‐induced HBE135‐E6E7 cell EMT model. (E and F) Fluorescence expression intensity of ITGA5 in the TGF ‐β 1‐induced HBE135‐E6E7 cell EMT model scale bar = 50 μm. (G) Protein interaction network of ITGA5 predicted by STRING. (H) Pro DIA‐based quantitative proteomics analysis process ( n = 5). (I) PCA analysis of all samples. (J) Volcano plot, red and green dots denote significantly up‐ and down‐regulated differentially expressed proteins (DEPs). DEPs identification criteria: | log 2 FC | ≥ 1 and p < 0.05. (K) GO enrichment analysis of DEPs, enrichment threshold: P < 0.05. (L) KEGG enrichment analysis of DEPs, enrichment threshold: P < 0.05. (M and N) Anoikis assay: Green calcein‐AM fluorescence (Ex = 485 nm, Em = 516 nm) indicates viable cells independent of adhesion, while red PI fluorescence (Ex = 535 nm, Em = 617 nm) indicates anoikis‐induced cell death. Scale bar: 100 μm. (O and P) Fluorescent intensity of the anoikis resistance marker TrkB. Scale bar: 50 μm. (Q and R) Protein levels of the anoikis resistance marker TrkB. Data were presented as mean ± SEM. n = 3 for each group. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001.

Journal: Cell Proliferation

Article Title: ITGA5 as a Dual Regulator of Epithelial‐Mesenchymal Transition and Epithelial Cell Anoikis Resistance: Functional Validation and Drug Prediction

doi: 10.1111/cpr.70190

Figure Lengend Snippet: TGF‐ β 1 induced EMT and anoikis resistance in human bronchial epithelial cells (HBE135‐E6E7). (Aand B) Western blot analysis of EMT phenotype markers (ZO‐1, E‐cadherin, Occludin, Fibronectin, N‐cadherin, Vimentin) at 48 h and 72 h, respectively. (C and D) Protein expression level of ITGA5 in the TGF‐ β 1‐induced HBE135‐E6E7 cell EMT model. (E and F) Fluorescence expression intensity of ITGA5 in the TGF ‐β 1‐induced HBE135‐E6E7 cell EMT model scale bar = 50 μm. (G) Protein interaction network of ITGA5 predicted by STRING. (H) Pro DIA‐based quantitative proteomics analysis process ( n = 5). (I) PCA analysis of all samples. (J) Volcano plot, red and green dots denote significantly up‐ and down‐regulated differentially expressed proteins (DEPs). DEPs identification criteria: | log 2 FC | ≥ 1 and p < 0.05. (K) GO enrichment analysis of DEPs, enrichment threshold: P < 0.05. (L) KEGG enrichment analysis of DEPs, enrichment threshold: P < 0.05. (M and N) Anoikis assay: Green calcein‐AM fluorescence (Ex = 485 nm, Em = 516 nm) indicates viable cells independent of adhesion, while red PI fluorescence (Ex = 535 nm, Em = 617 nm) indicates anoikis‐induced cell death. Scale bar: 100 μm. (O and P) Fluorescent intensity of the anoikis resistance marker TrkB. Scale bar: 50 μm. (Q and R) Protein levels of the anoikis resistance marker TrkB. Data were presented as mean ± SEM. n = 3 for each group. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001.

Techniques: Western Blot, Analysis, Expressing, Fluorescence, Quantitative Proteomics, Marker, Sample Prep, Protein Binding, Liquid Chromatography with Mass Spectroscopy, Tandem Mass Spectroscopy, Immunofluorescence

ITGA5 was associated with both TGF‐ β 1‐induced EMT and anoikis resistance in bronchial epithelial cells. (A) Venn plot of DEPs involved in EMT and anoikis resistance gene set identified 45 anoikis resistance‐related genes (ARRGs). (B) Radar plot of protein expression levels of ARRGs. (C) Co‐expression network of ARRGs. The size of the node represents the degree value. The larger the degree, the more genes interact with it. The connecting lines represent the correlation between ARRGs. The red line represents positive correlation and the blue line represents negative correlation. (D) Bubble plot of cell expression of ARRGs in healthy human lungs. (E) Pathway regulatory network of ARRGs. (F) Scatter plots of the correlation between ITGA5 and mesenchymal markers Fibronectin, N‐cadherin, Vimentin and epithelial marker E‐cadherin. (G) Biological process enrichment analysis of ITGA5‐high and ITGA5‐low groups, enrichment threshold: P < 0.05. (H) KEGG enrichment analysis of ITGA5‐high and ITGA5‐low groups, enrichment threshold: P < 0.05.

Journal: Cell Proliferation

Article Title: ITGA5 as a Dual Regulator of Epithelial‐Mesenchymal Transition and Epithelial Cell Anoikis Resistance: Functional Validation and Drug Prediction

doi: 10.1111/cpr.70190

Figure Lengend Snippet: ITGA5 was associated with both TGF‐ β 1‐induced EMT and anoikis resistance in bronchial epithelial cells. (A) Venn plot of DEPs involved in EMT and anoikis resistance gene set identified 45 anoikis resistance‐related genes (ARRGs). (B) Radar plot of protein expression levels of ARRGs. (C) Co‐expression network of ARRGs. The size of the node represents the degree value. The larger the degree, the more genes interact with it. The connecting lines represent the correlation between ARRGs. The red line represents positive correlation and the blue line represents negative correlation. (D) Bubble plot of cell expression of ARRGs in healthy human lungs. (E) Pathway regulatory network of ARRGs. (F) Scatter plots of the correlation between ITGA5 and mesenchymal markers Fibronectin, N‐cadherin, Vimentin and epithelial marker E‐cadherin. (G) Biological process enrichment analysis of ITGA5‐high and ITGA5‐low groups, enrichment threshold: P < 0.05. (H) KEGG enrichment analysis of ITGA5‐high and ITGA5‐low groups, enrichment threshold: P < 0.05.

Techniques: Expressing, Marker, Analysis

Journal: Cell Proliferation

Article Title: ITGA5 as a Dual Regulator of Epithelial‐Mesenchymal Transition and Epithelial Cell Anoikis Resistance: Functional Validation and Drug Prediction

doi: 10.1111/cpr.70190

Figure Lengend Snippet: Protein interaction analyses of ITGA5 with PI3K and TRKB and MD simulation of the Res‐ITGA5 complex. (A and B) Representative docked conformations of ITGA5 with PI3K and ITGA5 with TrkB, respectively. (C and D) Covariance matrices derived from NMA: Red regions denote positively correlated motions between residue pairs, whereas blue regions denote negatively correlated (anti‐correlated) motions. (E and F) Elastic network models illustrating the rigidity of interfacial atoms (grey regions), which resist deformation during collective motions. (G and H) SPR analysis of the protein–protein interaction between ITGA5 and PI3K. (I and K) Cellular expression localisation and fluorescence intensity of ITGA5 (green), PI3K (magenta), and TrkB (yellow). Scale bar: 10 μm. (L and M) Representative docking conformations of the Res‐ITGA5 complex, together with interaction mapping and hydrogen bond analysis. (N) RMSD plot of the Res‐ITGA5 complex. (O) RMSF analysis of the Res‐ITGA5 complex. (P) Binding energy profile of the Res‐ITGA5 complex, in which VDW represents van der Waals and hydrophobic interactions, ELE denotes electrostatic interactions, and Binding corresponds to the sum of VDW and ELE without considering solvation effects. (Q) Rg plot curve characteristics. Data were presented as mean ± SEM. n = 3 for each group. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001.

Techniques: Derivative Assay, Residue, Analysis, Expressing, Fluorescence, Docking Assay, Binding Assay, SPR Assay, Immunofluorescence

Effects of ITGA5 knockdown on TGF‐ β 1‐induced EMT, PI3K/Akt signalling, and anoikis resistance in bronchial epithelial cells. (A–H) Western blot analysis of protein expression levels of EMT markers (Fibronectin, N‐cadherin, E‐cadherin, Vimentin, ZO‐1 and Occludin) in TGF‐ β 1 stimulated cells following ITGA5 knockdown. (I–L) Western blot analysis of PI3K/Akt signalling axis proteins following ITGA5 knockdown. (M–S) Western blot analysis of anoikis resistance related proteins (XIAP, MCL‐1, TrkB, Caspase 3, Cleaved‐caspase 3, Caspase 9 and Cleaved‐caspase 9) after ITGA5 knockdown. (T–U) Anoikis assay post‐ITGA5 knockdown: Red PI fluorescence (Ex = 535 nm, Em = 617 nm) indicates anoikis‐induced cell death; scale bar: 100 μm. (V–X) Cellular spatial colocalisation and fluorescence intensity analyses of ITGA5 (green) with PI3K (magenta) and TrkB (yellow) after ITGA5 knockdown ( n = 3); scale bar: 10μm. Data were presented as mean ± SEM. n = 3 for each group. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001.

Journal: Cell Proliferation

Article Title: ITGA5 as a Dual Regulator of Epithelial‐Mesenchymal Transition and Epithelial Cell Anoikis Resistance: Functional Validation and Drug Prediction

doi: 10.1111/cpr.70190

Figure Lengend Snippet: Effects of ITGA5 knockdown on TGF‐ β 1‐induced EMT, PI3K/Akt signalling, and anoikis resistance in bronchial epithelial cells. (A–H) Western blot analysis of protein expression levels of EMT markers (Fibronectin, N‐cadherin, E‐cadherin, Vimentin, ZO‐1 and Occludin) in TGF‐ β 1 stimulated cells following ITGA5 knockdown. (I–L) Western blot analysis of PI3K/Akt signalling axis proteins following ITGA5 knockdown. (M–S) Western blot analysis of anoikis resistance related proteins (XIAP, MCL‐1, TrkB, Caspase 3, Cleaved‐caspase 3, Caspase 9 and Cleaved‐caspase 9) after ITGA5 knockdown. (T–U) Anoikis assay post‐ITGA5 knockdown: Red PI fluorescence (Ex = 535 nm, Em = 617 nm) indicates anoikis‐induced cell death; scale bar: 100 μm. (V–X) Cellular spatial colocalisation and fluorescence intensity analyses of ITGA5 (green) with PI3K (magenta) and TrkB (yellow) after ITGA5 knockdown ( n = 3); scale bar: 10μm. Data were presented as mean ± SEM. n = 3 for each group. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001.

Techniques: Knockdown, Western Blot, Analysis, Expressing, Fluorescence, Immunofluorescence

Res and M200 pharmacologically inhibited ITGA5 and ameliorated TGF‐ β 1–induced EMT in bronchial epithelium cells. (A and B) Cell viability of HBE135‐E6E7 cells following 48 h treatment with varying concentrations of Res or M200, as measured by CCK‐8 assay. (C–J) Res and M200 inhibited ITGA5 and improved the expression of EMT markers (Fibronectin, N‐cadherin, Vimentin, ZO‐1, E‐cadherin, and Occludin) proteins. Data were presented as mean ± SEM. n = 3 for each group. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001.

Journal: Cell Proliferation

Article Title: ITGA5 as a Dual Regulator of Epithelial‐Mesenchymal Transition and Epithelial Cell Anoikis Resistance: Functional Validation and Drug Prediction

doi: 10.1111/cpr.70190

Figure Lengend Snippet: Res and M200 pharmacologically inhibited ITGA5 and ameliorated TGF‐ β 1–induced EMT in bronchial epithelium cells. (A and B) Cell viability of HBE135‐E6E7 cells following 48 h treatment with varying concentrations of Res or M200, as measured by CCK‐8 assay. (C–J) Res and M200 inhibited ITGA5 and improved the expression of EMT markers (Fibronectin, N‐cadherin, Vimentin, ZO‐1, E‐cadherin, and Occludin) proteins. Data were presented as mean ± SEM. n = 3 for each group. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001.

Techniques: CCK-8 Assay, Expressing, Western Blot

Res and M200 inhibited ITGA5, suppressed PI3K/Akt pathway activation, and alleviated anoikis resistance. (A–D) Western blot analysis of PI3K/Akt signalling axis proteins in cells treated with Res or M200. (E–K) Western blot analysis of anoikis resistance related proteins (XIAP, MCL‐1, TrkB, Caspase 3, Cleaved‐caspase 3, Caspase 9 and Cleaved‐caspase 9) in cells treated with Res or M200. (L and M) Effects of Res and M200 on anoikis: Green calcein‐AM fluorescence (Ex = 485 nm, Em = 516 nm) indicates viable cells independent of adhesion, red PI fluorescence (Ex = 535 nm, Em = 617 nm) marked anoikis‐induced cell death, scale bar: 100 μm. (N–P) Spatial colocalisation and fluorescence intensity analyses of ITGA5 (green) with PI3K (magenta) and TrkB (yellow); scale bar: 10 μm. Data were presented as mean ± SEM. n = 3 for each group. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001.

Journal: Cell Proliferation

Article Title: ITGA5 as a Dual Regulator of Epithelial‐Mesenchymal Transition and Epithelial Cell Anoikis Resistance: Functional Validation and Drug Prediction

doi: 10.1111/cpr.70190

Figure Lengend Snippet: Res and M200 inhibited ITGA5, suppressed PI3K/Akt pathway activation, and alleviated anoikis resistance. (A–D) Western blot analysis of PI3K/Akt signalling axis proteins in cells treated with Res or M200. (E–K) Western blot analysis of anoikis resistance related proteins (XIAP, MCL‐1, TrkB, Caspase 3, Cleaved‐caspase 3, Caspase 9 and Cleaved‐caspase 9) in cells treated with Res or M200. (L and M) Effects of Res and M200 on anoikis: Green calcein‐AM fluorescence (Ex = 485 nm, Em = 516 nm) indicates viable cells independent of adhesion, red PI fluorescence (Ex = 535 nm, Em = 617 nm) marked anoikis‐induced cell death, scale bar: 100 μm. (N–P) Spatial colocalisation and fluorescence intensity analyses of ITGA5 (green) with PI3K (magenta) and TrkB (yellow); scale bar: 10 μm. Data were presented as mean ± SEM. n = 3 for each group. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001.

Techniques: Activation Assay, Western Blot, Analysis, Fluorescence, Immunofluorescence

Elevated ITGA5 expression in asthma mice lungs accompanied by upregulation of the PI3K/Akt pathway and anoikis resistance marker TrkB. (A–F) Western blot analysis of ITGA5, PI3K/Akt signalling–related proteins and anoikis resistance–associated proteins (XIAP and MCL‐1) in lung tissues of asthma mice. n = 3 for each group. (G–H) Immunohistochemical analysis of ITGA5 localisation and expression in lung tissues of asthma mice. n = 6 for each group. Scale bars: 200 and 50 μm. (I–J) Immunohistochemical analysis of TrkB localisation and expression in lung tissues of asthma mice. n = 6 for each group. Scale bars: 200 and 50 μm. Data are presented as mean ± SEM. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001.

Journal: Cell Proliferation

Article Title: ITGA5 as a Dual Regulator of Epithelial‐Mesenchymal Transition and Epithelial Cell Anoikis Resistance: Functional Validation and Drug Prediction

doi: 10.1111/cpr.70190

Figure Lengend Snippet: Elevated ITGA5 expression in asthma mice lungs accompanied by upregulation of the PI3K/Akt pathway and anoikis resistance marker TrkB. (A–F) Western blot analysis of ITGA5, PI3K/Akt signalling–related proteins and anoikis resistance–associated proteins (XIAP and MCL‐1) in lung tissues of asthma mice. n = 3 for each group. (G–H) Immunohistochemical analysis of ITGA5 localisation and expression in lung tissues of asthma mice. n = 6 for each group. Scale bars: 200 and 50 μm. (I–J) Immunohistochemical analysis of TrkB localisation and expression in lung tissues of asthma mice. n = 6 for each group. Scale bars: 200 and 50 μm. Data are presented as mean ± SEM. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001.

Techniques: Expressing, Marker, Western Blot, Analysis, Immunohistochemical staining, Immunohistochemistry

Res and M200 inhibited ITGA5 in vivo and reversed EMT in the lungs of asthma mice. (A–C) Immunofluorescence analysis of the colocalisation and expression of ITGA5, PI3K, and TrkB with the airway epithelial marker EpCAM in the lungs of asthma mice after treatment with Res and M200. n = 6 for each group. Scale bars: 50 and 20 μm. (D–J) Western blot analysis of the protein levels of EMT‐related markers (Fibronectin, N‐cadherin, Vimentin, ZO‐1, E‐cadherin, and Occludin) in lung tissues from asthma mice. n = 3 for each group. Data are presented as mean ± SEM. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001.

Journal: Cell Proliferation

Article Title: ITGA5 as a Dual Regulator of Epithelial‐Mesenchymal Transition and Epithelial Cell Anoikis Resistance: Functional Validation and Drug Prediction

doi: 10.1111/cpr.70190

Figure Lengend Snippet: Res and M200 inhibited ITGA5 in vivo and reversed EMT in the lungs of asthma mice. (A–C) Immunofluorescence analysis of the colocalisation and expression of ITGA5, PI3K, and TrkB with the airway epithelial marker EpCAM in the lungs of asthma mice after treatment with Res and M200. n = 6 for each group. Scale bars: 50 and 20 μm. (D–J) Western blot analysis of the protein levels of EMT‐related markers (Fibronectin, N‐cadherin, Vimentin, ZO‐1, E‐cadherin, and Occludin) in lung tissues from asthma mice. n = 3 for each group. Data are presented as mean ± SEM. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001.

Techniques: In Vivo, Immunofluorescence, Analysis, Expressing, Marker, Western Blot

(A) Representative hematoxylin-eosin (HE) staining images of MMD and CTRL arteries, showing characteristic medial thinning and intimal hyperplasia, and based on this, a spatial omics ROI analysis was designed. (B-C) Volcano plots and corresponding heatmaps of differentially expressed genes (DEGs) and differentially expressed proteins (DEPs) between the intima and media of MMD arteries. FN1 , ITGA5 , and FAK are significantly upregulated in the intima. (D) Violin plot quantifying the Intima/Media Area Ratio in MMD versus CTRL groups (****p < 0.0001). (E) Representative IF staining of ITGA5 (green) demonstrating its robust accumulation in the thickened intima of MMD compared to CTRL. (F-H) Scratch wound-healing assay and quantification of relative migration ability in VSMCs treated with 10 μg/mL FN1, showing that FN1-induced hyper-migration is significantly abrogated by ITGA5 knockdown (shRNA-ITGA5) or FAK inhibition (VS6063).

Journal: bioRxiv

Article Title: Spatial Multi-Omics Reveals Extracellular Matrix Remodeling and VSMC Phenotypic Switching in Moyamoya Disease

doi: 10.64898/2026.04.27.721225

Figure Lengend Snippet: (A) Representative hematoxylin-eosin (HE) staining images of MMD and CTRL arteries, showing characteristic medial thinning and intimal hyperplasia, and based on this, a spatial omics ROI analysis was designed. (B-C) Volcano plots and corresponding heatmaps of differentially expressed genes (DEGs) and differentially expressed proteins (DEPs) between the intima and media of MMD arteries. FN1 , ITGA5 , and FAK are significantly upregulated in the intima. (D) Violin plot quantifying the Intima/Media Area Ratio in MMD versus CTRL groups (****p < 0.0001). (E) Representative IF staining of ITGA5 (green) demonstrating its robust accumulation in the thickened intima of MMD compared to CTRL. (F-H) Scratch wound-healing assay and quantification of relative migration ability in VSMCs treated with 10 μg/mL FN1, showing that FN1-induced hyper-migration is significantly abrogated by ITGA5 knockdown (shRNA-ITGA5) or FAK inhibition (VS6063).

Article Snippet: The sections were then incubated overnight at 4°C with the following primary antibodies: anti-alpha Smooth Muscle Actin (alpha-SMA) (ab5694, Abcam; 1:200 dilution), anti-Integrin alpha 5 (ITGA5) (A19069, ABclonal; 1:200 dilution).

Techniques: Staining, Wound Healing Assay, Migration, Knockdown, shRNA, Inhibition

(A) Workflow for the generation of induced pluripotent stem cells (iPSCs) from peripheral blood mononuclear cells (PBMCs) of MMD patients and healthy controls (HC), followed by directed differentiation into VSMCs. (B-C) Representative images and quantification of Transwell migration assays. MMD-iPSC-SMCs exhibit significantly enhanced migration compared to HC-iPSC-SMCs, which is effectively reversed by shRNA-ITGA5 or VS6063 treatment. (D-F) Western blot analysis and quantification of total FAK and phosphorylated FAK (p-FAK at Tyr397) in the established iPSC-SMC models. The elevated p-FAK/FAK ratio in MMD-iPSC-SMCs is substantially reduced by ITGA5 silencing or direct FAK inhibition.

Journal: bioRxiv

Article Title: Spatial Multi-Omics Reveals Extracellular Matrix Remodeling and VSMC Phenotypic Switching in Moyamoya Disease

doi: 10.64898/2026.04.27.721225

Figure Lengend Snippet: (A) Workflow for the generation of induced pluripotent stem cells (iPSCs) from peripheral blood mononuclear cells (PBMCs) of MMD patients and healthy controls (HC), followed by directed differentiation into VSMCs. (B-C) Representative images and quantification of Transwell migration assays. MMD-iPSC-SMCs exhibit significantly enhanced migration compared to HC-iPSC-SMCs, which is effectively reversed by shRNA-ITGA5 or VS6063 treatment. (D-F) Western blot analysis and quantification of total FAK and phosphorylated FAK (p-FAK at Tyr397) in the established iPSC-SMC models. The elevated p-FAK/FAK ratio in MMD-iPSC-SMCs is substantially reduced by ITGA5 silencing or direct FAK inhibition.

Techniques: Migration, shRNA, Western Blot, Inhibition

Blocking the ITGA5 pathway may reduce the pathological phenotypic transformation of MMD-iPSC-SMC. (A) Representative Western blot images showing the expression levels of SMC contractile markers, synthetic/matrix markers, and ITGA5 in HC-iPSC-SMCs and MMD-iPSC-SMCs under various treatments. (B-D) Quantification of contractile markers (MYH11, CNN1, TAGLN). Expression is significantly loss in MMD-iPSC-SMCs but rescued upon treatment with shRNA-ITGA5 or VS6063. (E-J) Quantification of synthetic and extracellular matrix-related proteins (FN1, COL1A1, COL3A1, OGN, EFEMP1) and ITGA5. The abnormal upregulation of these markers in MMD-iPSC-SMCs is suppressed by targeting the ITGA5-FAK axis, indicating a reversal from the synthetic back to the contractile phenotype.

Journal: bioRxiv

Article Title: Spatial Multi-Omics Reveals Extracellular Matrix Remodeling and VSMC Phenotypic Switching in Moyamoya Disease

doi: 10.64898/2026.04.27.721225

Figure Lengend Snippet: Blocking the ITGA5 pathway may reduce the pathological phenotypic transformation of MMD-iPSC-SMC. (A) Representative Western blot images showing the expression levels of SMC contractile markers, synthetic/matrix markers, and ITGA5 in HC-iPSC-SMCs and MMD-iPSC-SMCs under various treatments. (B-D) Quantification of contractile markers (MYH11, CNN1, TAGLN). Expression is significantly loss in MMD-iPSC-SMCs but rescued upon treatment with shRNA-ITGA5 or VS6063. (E-J) Quantification of synthetic and extracellular matrix-related proteins (FN1, COL1A1, COL3A1, OGN, EFEMP1) and ITGA5. The abnormal upregulation of these markers in MMD-iPSC-SMCs is suppressed by targeting the ITGA5-FAK axis, indicating a reversal from the synthetic back to the contractile phenotype.

Techniques: Blocking Assay, Transformation Assay, Western Blot, Expressing, shRNA

(A) Representative spatial metabolomics mapping (m/z signals) showing the heterogeneous distribution of specific metabolites across different arterial segments. (B) 3D UMAP projection of spatial metabolic segments. (C-E) 2D Principal Component Analysis (PCA) plots distinguishing the distinct molecular signatures between MMD-MID-SMC (media) and MMD-IN-SMC (intima). (F-G) Multi-omics correlation heatmaps illustrating the strong spatial co-expression and inverse correlations between specific intimal genes/proteins (e.g., g.ITGA5 , p.Fibronectin ) and the abundance of localized metabolites. (H) Radar chart highlighting the top depleted compounds in the MMD intima compared to the media, revealing a profound exhaustion of Acyl-CoA derivatives (e.g., trans-Crotonyl CoA, 3-aminobutyryl-CoA).

Journal: bioRxiv

Article Title: Spatial Multi-Omics Reveals Extracellular Matrix Remodeling and VSMC Phenotypic Switching in Moyamoya Disease

doi: 10.64898/2026.04.27.721225

Figure Lengend Snippet: (A) Representative spatial metabolomics mapping (m/z signals) showing the heterogeneous distribution of specific metabolites across different arterial segments. (B) 3D UMAP projection of spatial metabolic segments. (C-E) 2D Principal Component Analysis (PCA) plots distinguishing the distinct molecular signatures between MMD-MID-SMC (media) and MMD-IN-SMC (intima). (F-G) Multi-omics correlation heatmaps illustrating the strong spatial co-expression and inverse correlations between specific intimal genes/proteins (e.g., g.ITGA5 , p.Fibronectin ) and the abundance of localized metabolites. (H) Radar chart highlighting the top depleted compounds in the MMD intima compared to the media, revealing a profound exhaustion of Acyl-CoA derivatives (e.g., trans-Crotonyl CoA, 3-aminobutyryl-CoA).

Techniques: Biomarker Discovery, Expressing

Journal: Advanced Science

Article Title: The Osteoblastic Microenvironment Determines the Fate of Breast Cancer Cells Disseminated in the Bone Marrow

doi: 10.1002/advs.202509980

Figure Lengend Snippet: RUNX2 increases the accumulation of MDA231 cells as micrometastases in bone marrow. (A) Experimental schedule for the bone colonization of MDA231‐derived cells in SCID mice. An osteogenic premetastatic niche (PMN) was established by injecting MDA231 CDH11 high /ITGA5 high extracellular vesicles into SCID mice via the tail vein for 3 weeks (2 doses/week). MDA231 RUNX2‐OE cells and control cells were injected into the mice via the left ventricle. (B) H&E staining images demonstrating osteoblasts (indicated by red triangles) in homeostatic bone (HB) and the PMN. (C) X‐ray images showing the bone mass in the HB and the PMN microenvironments. (D) Bar charts quantifying the osteoblast number as the ratio of osteoblast counts to bone perimeter in /mm (N.Ob/B.Pm) and bone mass as the bone volume fraction (BV/TV). (E) Western blot analysis demonstrating increased RUNX2 protein levels in MDA231 RUNX2‐OE cells compared with those in control cells. (F) Representative X‐ray images, pan‐cytokeratin (pan‐CK) immunohistochemical staining images, and TRAP staining images showing osteolytic lesions, tumor cell distribution, and activated osteoclasts, respectively. (G) Pie charts depicting the incidence of DTCs, micrometastases (micromets), and osteolytic lesions formed by control cells and RUNX2‐OE cells within HB and the PMN. The scale bars in the inset images indicate 20 µm. (H) Bar charts quantifying the tumor surface, erosion surface, and the number of TRAP + osteoclasts normalized to the total bone surface (N.Oc/BS in mm 2 ). (I) Bar charts illustrating the abundance and size of micrometastases in the bone marrow of mice without detectable bone lesions. (J) Representative KI67 fluorescence immunohistochemical staining images. Pan‐CK was used to label the tumor cells, while DAPI was used to stain the nuclei. (K) Bar chart illustrating the reduced numbers of KI67 + tumor cells in micrometastases compared with tumor cells within bone colonization. The data are displayed as the means ± SDs. n.s., not significant; * p <0.05, ** p <0.01, *** p <0.001 compared with the corresponding controls, as determined by Student's t‐test.

Article Snippet: Additionally, ATN‐161 (1 mg/kg, MCE, HY‐13535A) was employed to disrupt the tumor–bone matrix interaction mediated by ITGA5.

Techniques: Derivative Assay, Control, Injection, Staining, Western Blot, Immunohistochemical staining, Fluorescence

Journal: Advanced Science

Article Title: The Osteoblastic Microenvironment Determines the Fate of Breast Cancer Cells Disseminated in the Bone Marrow

doi: 10.1002/advs.202509980

Figure Lengend Snippet: The ITGA5 antagonist ATN‐161 reduces the incidence of bone colonization. (A–D) Experimental diagram (A), representative X‐ray, H&E staining, TRAP staining, and KI67 and pan‐CK immunofluorescence staining images (B), and bar charts demonstrating the inhibition of PTH‐reactivated bone colonization (C) and tumor surface normalized to the bone surface (D), in MDA231‐derived cells following ATN‐161 administration. (E–H) Experimental diagram (E), representative X‐ray, H&E staining, TRAP staining, and KI67 and pan‐CK immunofluorescence staining images (F), and bar charts displaying the blockade of E2‐supported bone colonization (G) and tumor surface normalized to the bone surface (H), in MCF7‐derived cells after ATN‐161 administration. The scale bars in the inset images indicate 20 µm. The data are presented as the means ± SDs. * p <0.05, ** p <0.01 compared with the respective control mice, as determined by Fisher's exact probability test or Student's t test.

Article Snippet: Additionally, ATN‐161 (1 mg/kg, MCE, HY‐13535A) was employed to disrupt the tumor–bone matrix interaction mediated by ITGA5.

Techniques: Staining, Immunofluorescence, Inhibition, Derivative Assay, Control

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