integrin α6  (R&D Systems)

Journal: Nature Communications

Article Title: Treg-γδ T cell axis determines sexual dimorphism in hepatocarcinogenesis

doi: 10.1038/s41467-026-69603-w

Figure Lengend Snippet: a Schematic flow of mouse orthotopic HCC implantation after gonadectomy. Liver SVG Vector by SVG Repo, licensed under CC0 1.0 Universal. Scissors SVG Vector by SVG Repo, licensed under CC0 1.0 Universal. b Representative flow plots (left) and quantification (right) of intratumoral Tregs after gonadectomy ( n = 5). c The relative mRNA expression of Ccl2 in orthotopic HCC measured by qPCR ( n = 5). d Representative immunofluorescent staining for AFP, Ccl2 and DAPI. scale bars, 50 μm (left). Quantification of AFP + Ccl2 + cells in HCC (right) ( n = 7). e HepG2 and Hepa1-6 cells were treated with testosterone (TS) at different concentrations. Representative fluorescence intensity plots (left) and quantification (right) of Ccl2 after treatment ( n = 4, 6). f The correlation analysis between the relative mRNA expression of CCL2 and NFKB1 in human HCC samples from the GEPIA database ( n = 398). g The immunoblots of Integrin α6, PAK1, AR, p-NFκB and NFκB ( n = 3). h–j Genetically deletion of AR in Hepa1-6 using CRISPR/Cas9 followed by orthotopic Hepa1-6 implantation. Representative liver image (left) and tumour volume (right) ( n = 5) ( h ). Representative immunofluorescent staining for AFP, Ccl2 and DAPI. scale bars, 50 μm (left). Quantification of Ccl2 intensity in HCC (right) ( n = 4) ( i ). Representative flow cytometry plots (left) and the statistical quantification (right) of Tregs ( n = 4) ( j ). Cut&Tag analysis was used to assess the interaction between NFκB and Ccl2 in HepG2 cells. Genomic Regions Enrichment of Annotations Tool (GREAT) (upper). Annotation of all peaks (lower) ( k , n = 3). The chromatin accessibility heatmap showing NFκB binding sequence regions with or without testosterone (TS) treatment (upper). Cut&Tag tracks of Ccl2 locus in HepG2 cells (lower) ( l , n = 3). Top2 de novo motifs (#1 and #2) of NFκB enriched by HOMER using all called peaks ( m , n = 3). The relative expression of Ccl2 with specific primers targeting motif #2 by qPCR ( n , n = 3). Data represent three independent experiments. Data are shown as the mean ± SEM. P value of Pearson r correlation ( f ) or one-way ANOVA followed by Bonferroni’s multiple comparisons test ( e and n ) or two-way ANOVA followed by Bonferroni’s multiple comparisons test ( b – d and h – j ). For additional details, see also Supplementary Fig. . Source data are provided as a Source Data file.

Article Snippet: The antibodies used were as follows: Integrin α6 (Huabio, SR45-00l, 1:1000), PAK1 (Baijia, IPB5302, 1:1000), Androgen receptor (Huabio, PO00-29, 1:1000), Phospho-NFκB p65 (Ser468, Proteintech, 6N1, 1:1000), NFκB p65 (Proteintech, 4C7, 1:1000), Hif1α (Servicebio, GB111339 , 1:1000), S100a4 (Huabio, SD200-08, 1:1000), HSP90 (Servicebio, GB15284, 1:1000), ZAP70 (Zenbio, R26132 , 1:1000), phospho-ZAP70 (Tyr319, Zenbio, 310211, 1:1000), Akt (HUABIO, ET1609-51, 1:1000), phospho-Akt (Ser473, SinoBiological, 110852-R0069, 1:1000), and Tubulin (Huabio, 1-B11, 1:5000).

Techniques: Plasmid Preparation, Expressing, Staining, Fluorescence, Western Blot, CRISPR, Flow Cytometry, Binding Assay, Sequencing

Journal: medRxiv

Article Title: A Three-subtype Molecular model of Cervical Cancer: Multiple PI3K Pathway inhibitors suppress growth and cooperate with HPV-directed immunotherapy

doi: 10.64898/2026.01.21.26344562

Figure Lengend Snippet: Impact of BYL-719 on the expression of target proteins in cervical cancer cell lines. (A, B) CaSki cells treated with BYL-719 show reduced levels of PD-L1, YAP1, EGFR, CTGF, Integrin, and HPV16 E7. In Panel B cells were treated with 5 uM BYL-719, washed at 24h and place in 0, 1 or 5 uM drug. (exposure time, 2 min). (C) BYL-719-treated ME180 cells show decreased levels of PD-L1 and CTGF. (D) SNU-17 cells also show reduced levels of these proteins after treatment (exposure time, 5 min). (E) SiHa (PIK3CA wild-type) shows no reduction in PD-L1 or HPV16 E7 after treatment with BYL-719 (exposure time, 3 minutes). (F) Cell proliferation plot of SNU-17 cells treated with BYL-719 (G). SiHa cells treated with BYL719. *=P<0.05, **=P< 0.01, ***=P<0.001.

Article Snippet: The primary antibodies used in this study were: rabbit monoclonal anti-PD-L1, (Cell Signaling Technology Cat# 13684, RRID: AB_2687655), YAP1, (Cell Signaling Technology Cat# 14074, RRID: AB_2650491), EGFR (Cell Signaling Technology Cat# 4267, RRID: AB_2800085), CTGF (Cell Signaling Technology Cat# 86641, RRID: AB_2800085), Integrin α6 (Cell Signaling Technology Cat# 3750, RRID: AB_2249263), IRF1 (Cell Signaling Technology Cat# 8478, RRID: AB_10949108) at a dilution of 1:500; mouse monoclonal anti-HPV16 E7 at 1:100 (Santa Cruz Cat# sc-51951, RRID: AB_629662), and goat monoclonal anti-p16 at 1:500 (R&D system Cat# AF5779, RRID: AB_1964666). β-actin, used as an internal control, was detected by rabbit anti-β-actin antibody (Cell Signaling Technology Cat# 4967, RRID: AB_330288).

Techniques: Expressing

Journal: Oncology Research

Article Title: INHBA Promotes the Progression of Gastric Cancer by Activating MAPK Signaling Pathway via Targeting ITGA6

doi: 10.32604/or.2025.070333

Figure Lengend Snippet: ITGA6 is the regulatory target of INHBA. ( A ) Differential expression genes (DEGs) heat map identified by RNA-seq. ( B ) The number of DEGs identified by RNA-seq. ( C ) Overlap analysis of RNA-seq and STAD-DEGs-up identified genes. ( D ) Expression of ITGA6 in GC paired tissue cohort from the GEPIA2 database. ( E ) Subcellular localization of ITGA6 from GeneCards. ( F , G ) The interaction between INHBA and ITGA6 was verified by Co-IF ( F ) and Co-IP ( G ) experiments. Scale bar, 50 μm. ( H ) qRT-PCR was used to detect ITGA6 mRNA expression after INHBA knockdown in NUGC-3 cells. ( I ) WB was used to detect ITGA6 protein expression after INHBA knockdown in NUGC-3 cells. ( J ) qRT-PCR was used to detect ITGA6 mRNA expression after INHBA overexpression in AGS cells. ( K ) WB was used to detect ITGA6 protein expression after INHBA overexpression in AGS cells. Data are presented as means ± SD. * p < 0.05, ** p < 0.01, **** p < 0.0001

Article Snippet: Primary INHBA antibody (diluted 1:50; Proteintech; Catalog number: 17524-1-AP) and ITGA6 antibody (diluted 1:50; Santa Cruz Biotechnology, Dallas, TX, USA; Catalog number: sc-374057) were added to the cells and incubated overnight at 4°C.

Techniques: Quantitative Proteomics, RNA Sequencing, Expressing, Co-Immunoprecipitation Assay, Quantitative RT-PCR, Knockdown, Over Expression

Journal: Oncology Research

Article Title: INHBA Promotes the Progression of Gastric Cancer by Activating MAPK Signaling Pathway via Targeting ITGA6

doi: 10.32604/or.2025.070333

Figure Lengend Snippet: Expression of ITGA6 and its interaction with INHBA in GC. ( A ) The basal expression of ITGA6 mRNA in GC cell lines and GES-1 was detected by qRT-PCR. ( B ) The basal expression of ITGA6 protein in cell lines was detected by WB. ( C ) The expression of ITGA6 protein in 30 pairs of GC paired tissues was detected by IHC. (magnification ×400). The red arrow indicates the ITGA6 expression area, which appears brown or yellow. ( D,E ) Four siRNA-ITGA6 sequences were transfected simultaneously into AGS cells. ( F,G ) The relative expression level of INHBA mRNA and protein was detected by qRT-PCR and WB after instantaneous co-transfection of INHBA siRNA and ITGA6 overexpression plasmid in NUGC-3. ( H,I ) The relative expression level of INHBA mRNA and protein were detected by qRT-PCR and WB after instantaneous co-transfection of ITGA6 siRNA and INHBA overexpression plasmid in AGS. Data are presented as means ± SD. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001

Article Snippet: Primary INHBA antibody (diluted 1:50; Proteintech; Catalog number: 17524-1-AP) and ITGA6 antibody (diluted 1:50; Santa Cruz Biotechnology, Dallas, TX, USA; Catalog number: sc-374057) were added to the cells and incubated overnight at 4°C.

Techniques: Expressing, Quantitative RT-PCR, Transfection, Cotransfection, Over Expression, Plasmid Preparation

Journal: Oncology Research

Article Title: INHBA Promotes the Progression of Gastric Cancer by Activating MAPK Signaling Pathway via Targeting ITGA6

doi: 10.32604/or.2025.070333

Figure Lengend Snippet: Oncogenic function of INHBA depends on ITGA6 and the MAPK signaling pathway. ( A ) KEGG enrichment result of the differentially expressed gene sets from the GEPIA2 database. ( B ) The expression levels of MAPK signaling pathway-related proteins were detected by WB after instantaneous co-transfection of INHBA siRNA and ITGA6 overexpression plasmid in NUGC-3. ( C,E,G,I,J ) The effects of ITGA6 on INHBA in NUGC-3 cells were detected by CCK-8 assay ( C ), colony formation assay ( E ), wound healing assay ( G ), Scale bar, 200 μm, Transwell migration assay ( I ) and Transwell invasion assay ( J ). Scale bar, 100 μm. ( D,F,H,K,L ) The effects of ITGA6 on INHBA in AGS cells were detected by CCK-8 assay ( D ), colony formation assay ( F ), wound healing assay ( H ), Scale bar, 200 μm, Transwell migration assay ( K ) and Transwell invasion assay ( L ). Scale bar, 100 μm. Data are presented as means ± SD. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001

Article Snippet: Primary INHBA antibody (diluted 1:50; Proteintech; Catalog number: 17524-1-AP) and ITGA6 antibody (diluted 1:50; Santa Cruz Biotechnology, Dallas, TX, USA; Catalog number: sc-374057) were added to the cells and incubated overnight at 4°C.

Techniques: Expressing, Cotransfection, Over Expression, Plasmid Preparation, CCK-8 Assay, Colony Assay, Wound Healing Assay, Transwell Migration Assay, Transwell Invasion Assay