Journal: Stem Cell Research & Therapy

Article Title: CD26 is a senescence marker associated with reduced immunopotency of human adipose tissue-derived multipotent mesenchymal stromal cells

doi: 10.1186/s13287-022-03026-4

Figure Lengend Snippet: Late passage (LP) MSC(AT) have a senescent transcriptome signature. A Gene set enrichment analysis demonstrates increased expression of genes known to be upregulated in senescence (shown in red) and reduced expression of genes downregulated in senescence (shown in blue) in LP-MSC(AT) and shows DPP4 among core enrichment genes; n = 1 pediatric and n = 1 adult, where EP = p6 and LP = p30. B – G Relative expression of selected transcripts from RNAseq analysis tested by quantitative RT-PCR over HPRT housekeeping gene in 9 additional samples. Expression of B CDKN2A (p16), C CDKN1A (p21), D DPP4 ( CD26), E HES1 , F SPP1 and G COL4A1 over the house-keeping gene HPRT . Data presented as mean ± SD, comparisons done with paired Wilcoxon test, * p < 0.05, ** p < 0.01

Article Snippet: The following primary antibodies were used at the dilutions indicated: CD26 (OriGene Technologies Inc., MD, USA; diluted 1:500), β-actin (Chemicon MAB1501; diluted 1: 100,000).

Techniques: Expressing, Quantitative RT-PCR

Journal: Stem Cell Research & Therapy

Article Title: CD26 is a senescence marker associated with reduced immunopotency of human adipose tissue-derived multipotent mesenchymal stromal cells

doi: 10.1186/s13287-022-03026-4

Figure Lengend Snippet: CD26 surface levels and total protein abundance in MSC(AT) increase with replicative senescence and age. A Western Blot of CD26 protein levels in MSC(AT) extracts from early passage (EP) and late passage (LP) pediatric ( n = 2) and adult ( n = 3) samples. Data represent mean + SEM, comparisons done with two-tailed Student’s t -test, * p < 0.05; ** p < 0.01. B Representative immunohistochemistry image of CD26 protein abundance in EP and LP-MSC(AT). C CD26 geometric mean fluorescence intensity (gMFI) and % CD26 high MSCs in EP and LP-MSC(AT) (6 adult and 4 pediatric MSC(AT), at EP = p4.1 ± 0.6 and LP = p21.0 ± 6.0). Data represent mean ± SD, comparisons done with paired Wilcoxon tests, ** p < 0.01. D CD26 gMFI and % CD26 high MSC(AT) in EP-MSC(AT) from pediatric and adult donors (6 pediatric MSC(AT) at p = 4.7 ± 0.5 and 6 adult MSC(AT) p = 3.8 ± 0.4). Data represent mean ± SD, comparisons done with unpaired Mann–Whitney tests, ** p < 0.01

Article Snippet: The following primary antibodies were used at the dilutions indicated: CD26 (OriGene Technologies Inc., MD, USA; diluted 1:500), β-actin (Chemicon MAB1501; diluted 1: 100,000).

Techniques: Western Blot, Two Tailed Test, Immunohistochemistry, Fluorescence, MANN-WHITNEY

Journal: Stem Cell Research & Therapy

Article Title: CD26 is a senescence marker associated with reduced immunopotency of human adipose tissue-derived multipotent mesenchymal stromal cells

doi: 10.1186/s13287-022-03026-4

Figure Lengend Snippet: CD26 high MSC(AT) are less immunosuppressive than CD26 low MSC(AT). A Flow cytometry gating strategy for FACS separation of MSC(AT) based on CD26 surface abundance: CD26 low and CD26 high populations. B Immunopotency assay (i.e., MSC inhibition of proliferating CD4 + T cells). CD3CD28 activated T-cells were co-cultured with either CD26 low or CD26 high MSC(AT) at a 1:16 MSC:PBMC ratio. n = 4 adult and 1 pediatric MSC(AT). Data represent mean ± SD, comparisons done with paired Wilcoxon tests, * p < 0.05

Article Snippet: The following primary antibodies were used at the dilutions indicated: CD26 (OriGene Technologies Inc., MD, USA; diluted 1:500), β-actin (Chemicon MAB1501; diluted 1: 100,000).

Techniques: Flow Cytometry, Inhibition, Cell Culture

Journal: Stem Cell Research & Therapy

Article Title: CD26 is a senescence marker associated with reduced immunopotency of human adipose tissue-derived multipotent mesenchymal stromal cells

doi: 10.1186/s13287-022-03026-4

Figure Lengend Snippet: Viability and CD26 surface levels in late passage MSC(AT) decrease following senolytic treatment. A Cell viability of late passage MSC(AT) that were either treated with DMSO (vehicle control) or a senolytic: NAVI: navitoclax (20 μM), QUER: quercetin (+:400 and ++:800 μM) and DMAG: 17-DMAG (+:25.6 and ++:51.2 μM). B CD26 gMFI and C %CD26 high MSCs among living MSC(AT). [ n = 4 adult and 1 pediatric LP-MSC(AT)]. Data presented as mean ± SD, comparisons done with paired one-way ANOVA, * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001

Article Snippet: The following primary antibodies were used at the dilutions indicated: CD26 (OriGene Technologies Inc., MD, USA; diluted 1:500), β-actin (Chemicon MAB1501; diluted 1: 100,000).

Techniques:

Journal: Frontiers in Immunology

Article Title: Integrative pan-cancer analysis of dipeptidyl peptidase 4 with clinical and in vitro validation in prostate cancer

doi: 10.3389/fimmu.2026.1616889

Figure Lengend Snippet: The flow chart, differential expression analysis, ceRNA network construction, and PPI network construction. (A) The flow chart of our analysis. (B) Expression of DPP4 in 33 tumor types between normal tissues and tumor tissues. DPP4 expression was down-regulated in BRCA ( p < 0.001), CESC ( p < 0.05), CHOL ( p < 0.001), COAD ( p < 0.05), KICH ( p < 0.001), LUSC ( p < 0.001), PCPG ( p < 0.05), READ ( p < 0.01) and UCEC ( p < 0.01), while it was up-regulated in GBM ( p < 0.01), KIRC ( p < 0.001), KIRP ( p < 0.001), LIHC ( p < 0.001), LUAD ( p < 0.001), STAD ( p < 0.05) and THCA ( p < 0.001). (C) The ceRNA network of DPP4. There were three key miRNAs correlated with DPP4 and there were eight lncRNAs correlated with the key miRNAs. (D) The PPI network of DPP4. At the proteomic level, DPP4 was closely associated with FN1, CXCR4, CAV1, ITGB1, PTPRC, ADA, GCG, GIP, ACE2, and PRCP. ceRNA, competing endogenous RNA; lncRNA, long non-coding RNA; PPI, Protein-Protein Interaction. * p < 0.05, ** p < 0.01, *** p < 0.001.

Article Snippet: Primary antibodies against human DPP4 (1:200; Affinity Biosciences Cat# DF12387, RRID: AB_2845192) were then introduced, followed by secondary antibodies conjugated with horseradish peroxidase (HRP).

Techniques: Quantitative Proteomics, Expressing

Journal: Frontiers in Immunology

Article Title: Integrative pan-cancer analysis of dipeptidyl peptidase 4 with clinical and in vitro validation in prostate cancer

doi: 10.3389/fimmu.2026.1616889

Figure Lengend Snippet: Survival analysis and univariate Cox regression analysis in pan-cancer. (A) Survival analysis of DPP4 in pan-cancer. K-M survival curves indicated DPP4 was positively correlated with OS in KIRC ( p < 0.001), with DSS in KIRC ( p < 0.001), and with DFS in PRAD ( p < 0.001). (B) Univariate Cox model of OS. DPP4 expression was a risk factor in DLBC (HR = 2.757, 95%CI = 1.066-7.127, p = 0.036), LAML (HR = 2.757, 95%CI = 1.066-7.127, p = 0.036), LGG (HR = 3.474, 95%CI = 2.617-4.611, p < 0.001), and LUSC (HR = 1.118, 95%CI = 1.000-2.014, p < 0.049), and it was a protective factor in KIRC (HR = 0.787, 95%CI = 0.716-0.865, p < 0.001), KIRP (HR = 0.789, 95%CI = 0.675-0.921, p = 0.003), LUAD (HR = 0.911, 95%CI = 0.837-0.992, p = 0.031), THCA (HR = 0.701, 95%CI = 0.553-0.887, p = 0.003), and THYM (HR = 0.440, 95%CI = 0.233-0.830, p = 0.011). (C) Univariate Cox model of DFS. DPP4 expression was a risk factor in LGG (HR = 4.698, 95%CI = 1.068-20.654, p = 0.041) and UCS (HR = 1.542, 95%CI = 1.004-2.370, p = 0.048), while it was a protective factor in PRAD (HR = 0.727, 95%CI = 0.567-0.931, p = 0.012). (D) Univariate Cox model in DSS. DPP4 expression was a risk factor in LGG (HR = 3.573, 95%CI = 2.672-4.778, p < 0.001), BRCA (HR = 1.383, 95%CI = 1.133-1.689, p = 0.001), DLBC (HR = 7.111, 95%CI = 1.469-34.432, p = 0.015), and ACC (HR = 1.343, 95%CI = 1.036-1.742, p = 0.026), while it was a protective factor in KIRC (HR = 0.703, 95%CI = 0.630-0.784, p < 0.001), KIRP (HR = 0.706, 95%CI = 0.595-0.838, p < 0.001), THCA (HR = 0.593, 95%CI = 0.419-0.839, p = 0.003), and LUAD (HR = 0.872, 95%CI = 0.782-0.971, p = 0.013). (E) Univariate Cox model in PFS. DPP4 expression was a risk factor in LGG (HR = 2.442, 95%CI = 1.884-3.163, p < 0.001), PCPG (HR = 1.832, 95%CI = 1.041-3.226, p = 0.036), and LUSC (HR = 1.137, 95%CI = 1.005-1.285, p = 0.041), while it was a protective factor in KIRC (HR = 0.787, 95%CI = 0.717-0.864, p < 0.001), PRAD (HR = 0.736, 95%CI = 0.638-0.850, p < 0.001), KIRP (HR = 0.818, 95%CI = 0.711-0.942, p = 0.005), PAAD (HR = 0.794, 95%CI = 0.659-0.956, p = 0.015), and MESO (HR = 0.836, 95%CI = 0.716-0.976, p = 0.023). OS, Overall Survival; DFS, Disease-Free Survival; DSS, Disease-Specific Survival; PFS, Progression-Free Survival. *p < 0.05, **p < 0.01, ***p < 0.001 .

Article Snippet: Primary antibodies against human DPP4 (1:200; Affinity Biosciences Cat# DF12387, RRID: AB_2845192) were then introduced, followed by secondary antibodies conjugated with horseradish peroxidase (HRP).

Techniques: Expressing

Journal: Frontiers in Immunology

Article Title: Integrative pan-cancer analysis of dipeptidyl peptidase 4 with clinical and in vitro validation in prostate cancer

doi: 10.3389/fimmu.2026.1616889

Figure Lengend Snippet: Relationship of DPP4 expression with TME in pan-cancer. (A) Correlation of DPP4 expression with MSI. It was positively correlated with MSI in COAD ( p < 0.001), ESCA ( p < 0.05), and KIRC ( p < 0.01), while it was negatively related in DLBC ( p < 0.001), HNSC ( p < 0.05), LUSC ( p < 0.001), PRAD ( p < 0.01), SKCM ( p < 0.001), and UCS ( p < 0.05). (B) Correlation of DPP4 expression with TMB. It was positively correlated with TMB in LAML ( p < 0.01), SARC ( p < 0.05), ESCA ( p < 0.001), KIRP ( p < 0.001), COAD ( p < 0.01), UCEC ( p < 0.05), GBM ( p < 0.05), LIHC ( p < 0.05), and OV ( p < 0.05), while it was negatively correlated in THYM ( p < 0.001), LUSC ( p < 0.001), CESC ( p < 0.05), PRAD ( p < 0.001), BRCA ( p < 0.001), and LUAD ( p < 0.05). (C) The relationship between DPP4 expression and immune-related genes. There is a significant association between DPP4 expression and immune-related genes across various cancers, particularly with NRP1 and HHLA2. Additionally, the majority of immune genes showed a positive correlation with DPP4 expression in BLCA, BRCA, LGG, SKCM, and THCA. (D) In PRAD, DPP4 expression was positively correlated with T cells CD4 memory resting (R = 0.18, p < 0.001), while it was negatively correlated with T cells CD8 (R = -0.19, p < 0.001), and T cells regulatory (R = -0.19, p < 0.001). MSI, Microsatellite Instability; TMB, Tumor Mutation Burden; TME, Tumor Microenvironment. *p < 0.05, **p < 0.01, ***p < 0.001 .

Article Snippet: Primary antibodies against human DPP4 (1:200; Affinity Biosciences Cat# DF12387, RRID: AB_2845192) were then introduced, followed by secondary antibodies conjugated with horseradish peroxidase (HRP).

Techniques: Expressing, Mutagenesis

Journal: Frontiers in Immunology

Article Title: Integrative pan-cancer analysis of dipeptidyl peptidase 4 with clinical and in vitro validation in prostate cancer

doi: 10.3389/fimmu.2026.1616889

Figure Lengend Snippet: Drug sensitivity prediction for DPP4 in (A) CellMiner, (B) CTRP and (C) GDSC databases. The expression of DPP4 was negatively related with drug sensitivity of most drugs. However, several drugs were positively related with DPP4 expression, including perifosine and adavosertib from CellMiner, dasatinib and saracatinib from CTRP, and cetuximab and crizotinib from GDSC. (D) The molecular docking analysis of DPP4 and dasatinib. (E) The molecular docking analysis of DPP4 and midostaurin. (F) The molecular docking analysis of DPP4 and saracatinib. (G) The molecular docking analysis of DPP4 and selumetinib. The possible binding sites were illustrated. (H) RMSD values of the protein-ligand complexes over time. The DPP4-Saracatinib complex reached equilibrium after 20 ns, with its RMSD fluctuating around 2.2 Å. The DPP4-Selumetinib complex reached equilibrium after 20 ns, fluctuating around 4.1 Å. The DPP4-Dasatinib complex reached equilibrium after 20 ns, fluctuating around 2.0 Å. The DPP4-Midostaurin complex reached equilibrium after 30 ns, fluctuating around 2.2 Å. (I) Rg of the protein-ligand complexes over time. All complex systems exhibited only minor fluctuations throughout the simulation. (J) SASA of the protein-ligand complexes over time. The results indicate that the SASA of the complexes did not change significantly after ligand binding to DPP4. (K) RMSF of the protein-ligand complexes. The RMSF values for all complexes were relatively low, with most residues fluctuating below 3 Å. RMSD, Root Mean Square Deviation; RMSF, Root-Mean-Square Fluctuation; Rg, Radius of gyration; SASA, Solvent-Accessible Surface Area.

Article Snippet: Primary antibodies against human DPP4 (1:200; Affinity Biosciences Cat# DF12387, RRID: AB_2845192) were then introduced, followed by secondary antibodies conjugated with horseradish peroxidase (HRP).

Techniques: Expressing, Binding Assay, Ligand Binding Assay, Solvent

Journal: Frontiers in Immunology

Article Title: Integrative pan-cancer analysis of dipeptidyl peptidase 4 with clinical and in vitro validation in prostate cancer

doi: 10.3389/fimmu.2026.1616889

Figure Lengend Snippet: A single-cell transcriptomic atlas of DPP4 in prostate cancer. (A) UMAP dimension reduction plot exhibiting 386,664 single-cell transcriptomes across nine major cell lineages (B cell, DC, endothelial cell, epithelial cell, fibroblast, mast cell, mono_macro, NK cell, and T cell) and 18 minor subtypes (luminal, basal, NE, NK cell, CD4+ T cell, CD8+ T cell, B cell, plasma cell, monocyte, macrophage, cDC1, cDC2, pDC, mast cell, fibroblast, SMC, pericyte, and endothelial cell). (B) Bubble plots depicting the feature expression of different marker genes in nine major cell subtypes. (C) UMAP dimension reduction plots by Grade1-5. (D) Bar plot demonstrating that the proportion of epithelial cells varied greatly in different grades of prostate cancer. (E) Stacked bar plots highlighting the enrichment of upregulated DEGs in epithelial cells within non-metastatic prostate cancer. (F, G) DPP4 expression was exclusively expressed in luminal cells. (H) Violin plots comparing DPP4 expression levels across ISUP grades, showing significantly higher expression in low-grade groups (p < 0.001). (I) Violin plots showing DPP4 expression across clinical T stages, indicating a significant downregulation in advanced stages (p < 0.001). (J) The interaction network illustrating the cellular communications of DPP4+ epithelial cells. (K) Heatmap summarizing the total interaction numbers, highlighting that DPP4+ epithelial cells exhibit significant communication with fibroblasts. (L) Volcano plot showing genes significantly perturbed by virtual DPP4 knockout in epithelial cells. (M) Functional enrichment analysis of the significantly perturbed genes following virtual KO of DPP4. UMAP, Uniform Manifold Approximation and Projection; AJCC, American Joint Committee on Cancer; DEG, Differential Expressed Genes; KO, Knockout.

Article Snippet: Primary antibodies against human DPP4 (1:200; Affinity Biosciences Cat# DF12387, RRID: AB_2845192) were then introduced, followed by secondary antibodies conjugated with horseradish peroxidase (HRP).

Techniques: Single Cell, Clinical Proteomics, Expressing, Marker, Knock-Out, Functional Assay

Journal: Frontiers in Immunology

Article Title: Integrative pan-cancer analysis of dipeptidyl peptidase 4 with clinical and in vitro validation in prostate cancer

doi: 10.3389/fimmu.2026.1616889

Figure Lengend Snippet: Higher DPP4 expression was correlated with better prognosis in prostate cancer. (A) The inclusion and exclusion criteria of the cohort. (B) IHC scores revealed that normal tissue exhibited significantly higher DPP4 expression compared to tumor tissues ( p < 0.001). (C) Representative IHC images of both prostate cancer and normal tissues from the cohort demonstrated this difference visually. (D) The Chi square test showed that DPP4 expression was associated with WHO/ISUP grade ( p = 0.03). (E) The K-M survival curve indicated that higher DPP4 expression was not significantly correlated with OS and PFS ( p > 0.05). However, DPP4 expression tended to be a protective factor. (F) Multivariate Cox regression analysis indicated that high DPP4 expression was an independent protective factor for OS in prostate cancer patients (HR = 0.052, 95%CI = 0.0041 - 0.65, p = 0.02). IHC, Immunohistochemical; OS, Overall Survival; PFS, Progression-Free Survival.

Article Snippet: Primary antibodies against human DPP4 (1:200; Affinity Biosciences Cat# DF12387, RRID: AB_2845192) were then introduced, followed by secondary antibodies conjugated with horseradish peroxidase (HRP).

Techniques: Expressing, Immunohistochemical staining

Journal: Frontiers in Immunology

Article Title: Integrative pan-cancer analysis of dipeptidyl peptidase 4 with clinical and in vitro validation in prostate cancer

doi: 10.3389/fimmu.2026.1616889

Figure Lengend Snippet: Dasatinib and midostaurin regulated DPP4 expression. (A) IC50 of 22Rv1 and C4–2 treated with dasatinib tested by CCK-8 assays. (B) IC50 of 22Rv1 and C4–2 treated with midostarin tested by CCK-8 assays. (C) Dasatinib treatment significantly increased DPP4 expression in C4–2 cells ( p = 0.0042, primer 1; p = 0.0029, primer 2). In contrast, midostaurin treatment reduced DPP4 expression in both cell lines (C4-2: p = 0.0218, primer 1; 22Rv1: p = 0.0172, primer 1; p = 0.0002, primer 2). IC50, Half maximal inhibitory concentration; CCK-8, Cell Counting Kit-8.

Article Snippet: Primary antibodies against human DPP4 (1:200; Affinity Biosciences Cat# DF12387, RRID: AB_2845192) were then introduced, followed by secondary antibodies conjugated with horseradish peroxidase (HRP).

Techniques: Expressing, CCK-8 Assay, Concentration Assay, Cell Counting

Journal: Emerging Infectious Diseases

Article Title: Livestock Susceptibility to Infection with Middle East Respiratory Syndrome Coronavirus

doi: 10.3201/eid2302.161239

Figure Lengend Snippet: Presence of MERS-CoV receptor DPP4 (IHC) and of mucosubstances (PAS) in upper and lower respiratory tract tissues from sheep, pigs, llamas, and horses. A) In the nose, DPP4 (red cytoplasmic or membrane staining) was present on the lining epithelium of pigs, llamas, and horses but not sheep. PAS staining (magenta) demonstrated more mucous cells in the lining epithelium of sheep and horses and a layer of mucus on the lining epithelium of the horses. B) DPP4 (red cytoplasmic or membrane staining) was present on the lining epithelium of the trachea, bronchus/bronchioles, and alveoli in the pigs, llamas and horses but not in the sheep. Original magnification ×400 for all images. DPP4, dipeptidyl peptidase-4; IHC, immunohistochemistry; MERS-CoV, Middle East respiratory syndrome coronavirus; PAS, periodic acid–Schiff; term., terminal.

Article Snippet: In brief, we performed DPP4 IHC staining by using 5 μg/mL of polyclonal goat IgG anti-human DPP4 antibody (R&D Systems, Abingdon, UK) and peroxidase-labeled rabbit anti-goat IgG (1:200; DAKO; Agilent Technologies Company, Santa Clara, CA, USA) as a secondary antibody.

Techniques: Membrane, Staining, Immunohistochemistry

Journal: Journal of Pediatric Hematology/Oncology

Article Title: Chemotherapy-induced Alteration of SDF-1/CXCR4 Expression in Bone Marrow–derived Mesenchymal Stem Cells From Adolescents and Young Adults With Acute Lymphoblastic Leukemia

doi: 10.1097/mph.0000000000000220

Figure Lengend Snippet: FIGURE 3. Secretion and expression of SDF-1 in BM-MSCs. A, SDF-1 level was measured by enzyme-linked immunosorbent assay. (a) The bone marrow plasma level of SDF-1 in patients with ALL was significantly increased compared with that in healthy donors and ALL-c (*P < 0.05; n = 10). (b), The same difference was found when SDF-1 levels were measured in the supernatants of MSC cultures after incubation for 72 hours. B, Western blotting was performed to quantify total SDF-1 in the lysates of MSCs. SDF-1 expression in the MSCs of ALL was significantly higher than that in the MSCs of healthy donors and ALL-c. C, The difference was also found at the transcriptional level by real-time PCR (*P < 0.05, n = 10). D, Surface-CD26 expression on the MSCs from ALL patients measured by flow cytometry was significantly lower than that in healthy donors and ALL-c (*P < 0.05; n = 10). E, Total CD26 was measured by Western blot in the MSCs. The fold difference was shown among the 3 types of MSCs. F, The same difference was also found at the transcriptional level (*P < 0.05; n = 10). ALL indicates acute lymphoblastic leukemia; BM-MSC, bone marrow–derived mesenchymal stem cell; GADPH, glyceraldehyde- 3-phosphate dehydrogenase; PCR, polymerase chain reaction.

Article Snippet: Membranes were hybridized with the following primary antibodies: rabbit anti-human CXCR4 (1:1000; Abcam), goat antihuman SDF-1(1:500; R&D Systems), goat anti-human CD26 (1:1000; R&D Systems), and mouse antibody to glyceraldehyde-3-phosphate dehydrogenase (1:4000; Santa Cruz).

Techniques: Expressing, Enzyme-linked Immunosorbent Assay, Clinical Proteomics, Incubation, Western Blot, Real-time Polymerase Chain Reaction, Flow Cytometry, Derivative Assay, Polymerase Chain Reaction