Journal: Journal of Clinical Medicine

Article Title: Adiponectin Associates with Rheumatoid Arthritis Risk in Overweight and Obesity Independently of Other Adipokines

doi: 10.3390/jcm10132791

Figure Lengend Snippet: Baseline characteristics of the nested case-control cohort from the SOS study.

Article Snippet: Serum leptin, resistin, and visfatin levels were measured using Human Leptin Quantikine ELISA Kit (DLP00, Bio-Techne, Minneapolis, MN, USA), Human Resistin Quantikine ELISA Kit (DRSN00, Bio-Techne, Minneapolis, MN, USA), and Nampt (Visfatin/PBEF) human ELISA Kit (AG-45A-0006YEK-KI01, AdipoGen Life Sciences, San Diego, CA, USA) respectively, between April and June 2018 at the University of Gothenburg, Sweden.

Techniques:

Journal: Journal of Clinical Medicine

Article Title: Adiponectin Associates with Rheumatoid Arthritis Risk in Overweight and Obesity Independently of Other Adipokines

doi: 10.3390/jcm10132791

Figure Lengend Snippet: Baseline characteristics of the nested case-control cohort from the Medical Biobank of Northern Sweden.

Article Snippet: Serum leptin, resistin, and visfatin levels were measured using Human Leptin Quantikine ELISA Kit (DLP00, Bio-Techne, Minneapolis, MN, USA), Human Resistin Quantikine ELISA Kit (DRSN00, Bio-Techne, Minneapolis, MN, USA), and Nampt (Visfatin/PBEF) human ELISA Kit (AG-45A-0006YEK-KI01, AdipoGen Life Sciences, San Diego, CA, USA) respectively, between April and June 2018 at the University of Gothenburg, Sweden.

Techniques: Northern Blot

Journal: Journal of Clinical Medicine

Article Title: Adiponectin Associates with Rheumatoid Arthritis Risk in Overweight and Obesity Independently of Other Adipokines

doi: 10.3390/jcm10132791

Figure Lengend Snippet: Multivariable conditional logistic regression analysis for RA in the nested case-control cohort from the SOS study.

Article Snippet: Serum leptin, resistin, and visfatin levels were measured using Human Leptin Quantikine ELISA Kit (DLP00, Bio-Techne, Minneapolis, MN, USA), Human Resistin Quantikine ELISA Kit (DRSN00, Bio-Techne, Minneapolis, MN, USA), and Nampt (Visfatin/PBEF) human ELISA Kit (AG-45A-0006YEK-KI01, AdipoGen Life Sciences, San Diego, CA, USA) respectively, between April and June 2018 at the University of Gothenburg, Sweden.

Techniques:

Journal: Journal of Clinical Medicine

Article Title: Adiponectin Associates with Rheumatoid Arthritis Risk in Overweight and Obesity Independently of Other Adipokines

doi: 10.3390/jcm10132791

Figure Lengend Snippet: Multivariable conditional logistic regression analysis for RA risk (A) and logistic regression analyses after stratifying for BMI (B and C) in the Medical Biobank of Northern Sweden cohort.

Article Snippet: Serum leptin, resistin, and visfatin levels were measured using Human Leptin Quantikine ELISA Kit (DLP00, Bio-Techne, Minneapolis, MN, USA), Human Resistin Quantikine ELISA Kit (DRSN00, Bio-Techne, Minneapolis, MN, USA), and Nampt (Visfatin/PBEF) human ELISA Kit (AG-45A-0006YEK-KI01, AdipoGen Life Sciences, San Diego, CA, USA) respectively, between April and June 2018 at the University of Gothenburg, Sweden.

Techniques: Northern Blot

Journal: Journal of Clinical Medicine

Article Title: Adiponectin Associates with Rheumatoid Arthritis Risk in Overweight and Obesity Independently of Other Adipokines

doi: 10.3390/jcm10132791

Figure Lengend Snippet: Baseline characteristics of the cohort from the Medical Biobank of Northern Sweden stratified by BMI.

Article Snippet: Serum leptin, resistin, and visfatin levels were measured using Human Leptin Quantikine ELISA Kit (DLP00, Bio-Techne, Minneapolis, MN, USA), Human Resistin Quantikine ELISA Kit (DRSN00, Bio-Techne, Minneapolis, MN, USA), and Nampt (Visfatin/PBEF) human ELISA Kit (AG-45A-0006YEK-KI01, AdipoGen Life Sciences, San Diego, CA, USA) respectively, between April and June 2018 at the University of Gothenburg, Sweden.

Techniques: Northern Blot

Journal: Cell death & disease

Article Title: Deletion of Mettl3 in mesenchymal stem cells promotes acute myeloid leukemia resistance to chemotherapy.

doi: 10.1038/s41419-023-06325-7

Figure Lengend Snippet: Fig. 1 Deletion of Mettl3 in MSCs induces high marrow adiposity in mice. A Western blot analysis of METTL3 in BMMSCs isolated from mice. B Detections of m6A levels in total RNA in BMMSCs from mice using EpiQuik m6A RNA Methylation Quantification Kits. C Representative images of H&E staining and FABP4 immunohistochemical staining of the distal femora from mice. Scale Bars: 100 μm. D Quantification of adipocyte number and area per tissue area in the distal marrow (n = 8). E ELISA examined the contents of supernatant adipokines in bone marrow rinses of mice (n = 6). F Representative images and quantitative analyses of Alizarin Red Solution (ARS) staining of BMMSCs isolated from mice. Scale Bars: 200 μm. G Representative images and quantitative analyses of ORO staining of BMMSCs isolated from mice. Scale Bars: 200 μm. The data are presented as mean ± SD. The two-tailed unpaired Student’s t test was used to compare two groups and one-way ANOVA with Dunnett’s multiple comparisons test was used for data with more than two groups. *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001, ns not significant.

Article Snippet: In the supernatant, based on the Cell Death and Disease (2023) 14:796 manufacturer’s directions, the levels of adipokines, like resistin, leptin, and growth hormone, were quantified employing the kits of Mouse Resistin ELISA (Cat# CSB-E06886m, CUSABIO, Wuhan, Hubei, China), Mouse Leptin ELISA (Cat# CSB-E04650m, CUSABIO), and Mouse Growth Hormone ELISA (Cat# CSB-E07343m, CUSABIO), respectively.

Techniques: Western Blot, Isolation, Methylation, Staining, Immunohistochemical staining, Enzyme-linked Immunosorbent Assay, Two Tailed Test

Journal: Cell death & disease

Article Title: Deletion of Mettl3 in mesenchymal stem cells promotes acute myeloid leukemia resistance to chemotherapy.

doi: 10.1038/s41419-023-06325-7

Figure Lengend Snippet: Fig. 4 METTL3 deletion reduces AML chemosensitivity by inducing adipogenic differentiation of OP9 cells. A Representative images and quantification of ORO staining in Mettl3 overexpression cells after 14 days of adipogenic induction. Scale bar, 100 µm. B qPCR analysis of the expression of adipogenic marker genes, Adipoq, Cebpa, Lpl, Plin1, CD36, and Pparγ in Mettl3 overexpression cells under adipogenic conditions. C ORO staining of Mettl3 knockdown cells following adipogenic induction. Scale bar, 100 µm. Absorbance at OD500 was determined for ORO staining in isopropanol at room temperature. D qPCR analysis of adipogenic lineage–associated gene expression after induction of differentiation in Mettl3 knockdown cells. E ELISA detection of adipokine concentration in the culture medium before induction of differentiation and on day 14 of Mettl3 overexpression cells. F ELISA detection of adipokine concentration in the culture medium before induction of differentiation and on day 14 of Mettl3 knockdown cells. G After adipogenic differentiation of Mettl3 overexpression cells, AML cells were co-cultured with them for 24 h to test their chemoresistance to Ara-C and DNR. H After adipogenic differentiation of Mettl3 knockdown cells, AML cells were co-cultured with them for 24 h to test their chemoresistance to Ara-C and DNR. Blank, blank control; OE-NC, negative control of overexpression; Mettl3-OE, overexpression of mouse Mettl3; sh-NC, negative control of knockdown; shMettl3-1 and shMettl3-2, independent shRNAs targeting mouse Mettl3. The data are presented as mean ± SD. The two-tailed unpaired Student’s t test was used to compare two groups and one-way ANOVA with Dunnett’s multiple comparisons test was performed for multiple groups. *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001, ns not significant.

Article Snippet: In the supernatant, based on the Cell Death and Disease (2023) 14:796 manufacturer’s directions, the levels of adipokines, like resistin, leptin, and growth hormone, were quantified employing the kits of Mouse Resistin ELISA (Cat# CSB-E06886m, CUSABIO, Wuhan, Hubei, China), Mouse Leptin ELISA (Cat# CSB-E04650m, CUSABIO), and Mouse Growth Hormone ELISA (Cat# CSB-E07343m, CUSABIO), respectively.

Techniques: Staining, Over Expression, Expressing, Marker, Knockdown, Gene Expression, Enzyme-linked Immunosorbent Assay, Concentration Assay, Cell Culture, Control, Negative Control, Two Tailed Test

Journal: Cell death & disease

Article Title: Deletion of Mettl3 in mesenchymal stem cells promotes acute myeloid leukemia resistance to chemotherapy.

doi: 10.1038/s41419-023-06325-7

Figure Lengend Snippet: Fig. 6 AKT inhibitor MK2206 mediates the adipogenesis level of OP9 cells. A Western blot analysis of AKT and p-AKT1 (Ser473) in OP9 cells treated with MK2206, an AKT inhibitor. B ORO staining of DMSO and MK2206 treated cells after adipo-induced for 14 days. Scale bar, 100 μm. C ELISA detected the concentration of adipokines in the culture medium before induction of differentiation and on day 14 under treatment with MK2206. D After being treated with MK2206 for 18 h and adipo-induced for 14 days, co-culturing with AML cells for 24 h was performed to test the chemoresistance of AML cells to Ara-C and DNR. The data are presented as mean ± SD. The two-tailed unpaired Student’s t test was used to compare two groups and one-way ANOVA with Dunnett’s multiple comparisons test was performed for multiple groups. *P < 0.05, **P < 0.01, ***P < 0.001, ns not significant.

Article Snippet: In the supernatant, based on the Cell Death and Disease (2023) 14:796 manufacturer’s directions, the levels of adipokines, like resistin, leptin, and growth hormone, were quantified employing the kits of Mouse Resistin ELISA (Cat# CSB-E06886m, CUSABIO, Wuhan, Hubei, China), Mouse Leptin ELISA (Cat# CSB-E04650m, CUSABIO), and Mouse Growth Hormone ELISA (Cat# CSB-E07343m, CUSABIO), respectively.

Techniques: Western Blot, Staining, Enzyme-linked Immunosorbent Assay, Concentration Assay, Two Tailed Test

Journal: Journal of biomedical science

Article Title: Neutrophil-derived reactive agents induce a transient SpeB negative phenotype in Streptococcus pyogenes.

doi: 10.1186/s12929-023-00947-x

Figure Lengend Snippet: Fig. 1 Reversible loss of SpeB is associated with tissue pathology and inflammation. A Distribution of SpeB+ and SpeB− GAS clones directly isolated from NSTI patient tissue biopsies (n = 23). B Percentage of SpeB+ and SpeB− GAS clones after the passage in THY media (p1, passage 1; p2, passage 2). Representative analysis of 2006 GAS patient isolate is shown. C–G Correlation analysis of bacterial load (left panel; n = 81 biopsies) or percentage of SpeB− clones (right panel; n = 23 biopsies) with the presence of HMGB1 (C), IL-8 (D), infiltrating neutrophils (E), and resistin (F) in patient biopsies. Correlation was determined using Spearman test. Semiquantitative acquired computerized image analyses (ACIA) of immuno-histochemical staining were performed as described in the methods section. The cell area was defined by the hematoxylin counterstaining, and the results are presented as percent positively stained area × mean intensity of positive staining

Article Snippet: The following antibodies were used for immunohistochemistry: anti-human HMGB1 (clone EPR3507; Abcam), anti-human IL-8 (clone NAP-1; Invitrogen), anti-human resistin (clone 184,305; R&D systems), and anti-human neutrophilelastase (clone NP57; DAKO).

Techniques: Clone Assay, Isolation, Staining

Journal: The Journal of Clinical Hypertension

Article Title: Masked Hypertension and Atherogenesis: The Impact on Adiponectin and Resistin Plasma Levels

doi: 10.1111/j.1751-7176.2008.00070.x

Figure Lengend Snippet: Resistin and Adiponectin Plasma Levels of the Study Groups

Article Snippet: The adiponectin plasma levels (RD195023100; Human Adiponectin ELISA Bio Vendor Laboratory Medicine Inc, Brno, Czech Republic) and the resistin plasma levels (RD191016100; Human Resistin ELISA Bio Vendor Laboratory Medicine Inc.) were measured by immunoassay .

Techniques:

Journal: Scientific Reports

Article Title: ADSCs stimulated by resistin promote breast cancer cell malignancy via CXCL5 in a breast cancer coculture model

doi: 10.1038/s41598-022-19290-6

Figure Lengend Snippet: Enhanced malignant behaviors of breast cancer cells after co-culture with resistin-stimulated ADSCs. The isolated ADSCs were treated with resistin at 0, 50, and 100 ng/ml (R0, R50, and R100, respectively) for 48 h, followed by co-culture with MDA-MB-231 or MCF-7 cells in the transwell model for another 72 h before the following analyses. ( A ) MDA-MB-231 cells after co-culture with R-ADSCs (R50 and R100) or control ADSCs (R0) were collected and re-plated in 96-well plates for cell viability assay. ( B ) MDA-MB-231 or MCF-7 cells after co-culture with R-ADSCs (R50 and R100) or control ADSCs (R0) were collected and re-plated in the transwell inserts for cell migration assay. ( C ) MDA-MB-231 or MCF-7 cells after co-culture with R-ADSCs (R50 and R100) or control ADSCs (R0) were collected and re-plated in the transwell inserts coated with Matrigel for cell invasion assay. ( D ) MDA-MB-231 or MCF-7 cells after co-culture with R-ADSCs (R50) or control ADSCs (R0) were collected and re-plated in ultra-low attachment microplates for tumorsphere formation assay. Quantitation was carried out for those with diameter over 50 μm. ( E ) MDA-MB-231 cells after co-culture with R-ADSCs (R50 and R100) or control ADSCs (R0) were collected and analyzed for protein expression of mesenchymal markers (Slug, Snail, and Vimentin) and cancer stemness markers (Nanog and Oct4) by Western blot. The original blot images were available in Supplementary Information, and these blots were cut from full-length membranes prior to hybridization with the corresponding antibodies. Data were obtained from three independent experiments and presented as mean ± SEM. Statistical difference was determined by t-test comparing R50 or R100 group versus their corresponding R0 group as control. * p < 0.05; ** p < 0.01; *** p < 0.001.

Article Snippet: The primary antibodies used in this study for IHC are listed as follows: rabbit polyclonal antibody against human Slug (GeneTex, Hsinchu, Taiwan); goat polyclonal antibody against human CXCL5 (R&D Systems, Minneapolis, MN, USA); mouse monoclonal antibody against human resistin (clone C-10; Santa Cruz Biotechnology, Dallas, TX, USA); rabbit monoclonal antibody against human phosphorylated ERK1/2 at Thr202/Tyr204 (clone D13.14.4E; Cell Signaling Technology, Danvers, MA, USA).

Techniques: Co-Culture Assay, Isolation, Control, Viability Assay, Cell Migration Assay, Invasion Assay, Tube Formation Assay, Quantitation Assay, Expressing, Western Blot, Hybridization

Journal: Scientific Reports

Article Title: ADSCs stimulated by resistin promote breast cancer cell malignancy via CXCL5 in a breast cancer coculture model

doi: 10.1038/s41598-022-19290-6

Figure Lengend Snippet: Secreted CXCL5 in the conditioned medium of the co-culture model with resistin-stimulated ADSCs promoted malignant behaviors of breast cancer cells. The isolated ADSCs were treated with resistin at 0 and 100 ng/ml (R0 and R100, respectively) for 48 h, followed by co-culture with MDA-MB-231 cells in the transwell model for another 72 h before the analyses in (A,B,F,G). ( A ) The conditioned medium from the co-culture of R-ADSCs (R100) or control ADSCs (R0) with MDA-MB-231 cells was collected and analyzed by cytokine/chemokine proteome array. A total of 102 proteins were detected with duplicates for each protein. The position of CXCL5 on the array was highlighted. ( B ) Secreted protein level of CXCL5 in the conditioned medium from the co-culture of R-ADSCs (R100) or control ADSCs (R0) with MDA-MB-231 cells was analyzed by ELISA. ( C ) MDA-MB-231 cells treated with recombinant CXCL5 (0, 20, and 40 ng/ml) for 48 h were collected and evaluated by cell migration assay. ( D ) MDA-MB-231 cells treated with recombinant CXCL5 (0, 20, and 40 ng/ml) for 48 h were collected and evaluated by cell invasion assay. ( E ) MDA-MB-231 cells treated with recombinant CXCL5 (0, 20, and 40 ng/ml) for 48 h were collected and analyzed for the protein expression of mesenchymal marker Slug and cancer stemness marker Oct4 by Western blot. The original blot images in (A) and (E) were available in Supplementary Information. ( F,G ) CXCL5 neutralizing antibody was added ( +) or omitted (–) during the co-culture of R-ADSCs (R100) or control ADSCs (R0) with MDA-MB-231 cells. After the co-culture, MDA-MB-231 cells were collected and evaluated by cell migration assay in (F) and cell invasion assay in (G). Data were obtained from three independent experiments and presented as mean ± SEM. Statistical difference was determined by t-test comparing R100 group versus their corresponding R0 group as control, or comparing recombinant CXCL5 treatment group (20 and 40 ng/ml) versus recombinant CXCL5 control group (0 ng/ml). * p < 0.05; ** p < 0.01; *** p < 0.001.

Article Snippet: The primary antibodies used in this study for IHC are listed as follows: rabbit polyclonal antibody against human Slug (GeneTex, Hsinchu, Taiwan); goat polyclonal antibody against human CXCL5 (R&D Systems, Minneapolis, MN, USA); mouse monoclonal antibody against human resistin (clone C-10; Santa Cruz Biotechnology, Dallas, TX, USA); rabbit monoclonal antibody against human phosphorylated ERK1/2 at Thr202/Tyr204 (clone D13.14.4E; Cell Signaling Technology, Danvers, MA, USA).

Techniques: Co-Culture Assay, Isolation, Control, Enzyme-linked Immunosorbent Assay, Recombinant, Cell Migration Assay, Invasion Assay, Expressing, Marker, Western Blot

Journal: Scientific Reports

Article Title: ADSCs stimulated by resistin promote breast cancer cell malignancy via CXCL5 in a breast cancer coculture model

doi: 10.1038/s41598-022-19290-6

Figure Lengend Snippet: ERK phosphorylation in breast cancer cells after co-culture with resistin-stimulated ADSCs mediated the cancer cell migration ability. The isolated ADSCs were treated with resistin at 0 and 50 ng/ml (denoted as R0 and R50, respectively) for 48 h, followed by co-culture with breast cancer cells in the transwell model for another 72 h before the following analyses. ( A ) Total protein lysates from MDA-MB-231 cells after co-culture with R-ADSCs (R50) or control ADSCs (R0) were collected and analyzed by phospho-kinase proteome array. A total of 43 phosphorylation sites were detected with duplicates for each protein. The position of phospho-ERK1/2 (p-ERK1/2) on the array was highlighted. ( B ) MDA-MB-231 cells after co-culture with R-ADSCs (R50) or control ADSCs (R0) were collected and analyzed for the protein expression of phospho-ERK1/2 and total ERK1/2 by Western blot. The original blot images in (A) and (B) were available in Supplementary Information. ( C ) PD98059 (5 μM) was added (+) or omitted (–) during the co-culture of MDA-MB-231 with R-ADSCs (R50) or control ADSCs (R0). After the co-culture, MDA-MB-231 cells were collected and evaluated by cell migration assay. Data were obtained from three independent experiments and presented as mean ± SEM. Statistical difference was determined by t-test comparing R50 group versus R0 group as control, or comparing R50 group with PD98059 ( +) versus R50 group without PD98059 (–). * p < 0.05; ** p < 0.01.

Article Snippet: The primary antibodies used in this study for IHC are listed as follows: rabbit polyclonal antibody against human Slug (GeneTex, Hsinchu, Taiwan); goat polyclonal antibody against human CXCL5 (R&D Systems, Minneapolis, MN, USA); mouse monoclonal antibody against human resistin (clone C-10; Santa Cruz Biotechnology, Dallas, TX, USA); rabbit monoclonal antibody against human phosphorylated ERK1/2 at Thr202/Tyr204 (clone D13.14.4E; Cell Signaling Technology, Danvers, MA, USA).

Techniques: Phospho-proteomics, Co-Culture Assay, Migration, Isolation, Control, Expressing, Western Blot, Cell Migration Assay

Journal: Scientific Reports

Article Title: ADSCs stimulated by resistin promote breast cancer cell malignancy via CXCL5 in a breast cancer coculture model

doi: 10.1038/s41598-022-19290-6

Figure Lengend Snippet: Enhanced breast tumor growth and protein expression of CXCL5, Slug, and ERK phosphorylation in mice via xenograft of breast cancer cells after co-culture with resistin-stimulated ADSCs. The isolated ADSCs were treated with resistin at 0 and 50 ng/ml (denoted as R0 and R50, respectively) for 48 h, followed by co-culture with MDA-MB-231 cells in the transwell model for another 72 h. After the co-culture, MDA-MB-231 cells were collected and injected into the fourth mammary fat pads of female NOD/SCID mice for the following analyses. ( A ) The tumor volume, calculated by (width 2 × length)/2, was measured weekly after palpable tumor mass was formed. ( B ) Upon sacrifice of the mice on week eight, the weight of individual tumor mass was measured. ( C ) The body weight of the mice was measured weekly. ( D ) The tumor mass was collected after sacrifice of the mice on week eight, and analyzed for CXCL5, Slug, and phospho-ERK1/2 protein expression by immunohistochemistry (IHC). The quantitative IHC scores were manually evaluated and calculated by multiplying the categorized percentage of stained cells (0, 0–24%; 1, 25‑49%; 2, 50‑74%; 3, 75‑100%) by the categorized intensity of staining (0, negative; 1, weak; 2, moderate; 3, strong). Data were obtained from three to six mice in each group and presented as mean ± SEM or box plots. Statistical difference was determined by t-test comparing R50 group versus R0 group as control. * p < 0.05; ** p < 0.01; *** p < 0.001.

Article Snippet: The primary antibodies used in this study for IHC are listed as follows: rabbit polyclonal antibody against human Slug (GeneTex, Hsinchu, Taiwan); goat polyclonal antibody against human CXCL5 (R&D Systems, Minneapolis, MN, USA); mouse monoclonal antibody against human resistin (clone C-10; Santa Cruz Biotechnology, Dallas, TX, USA); rabbit monoclonal antibody against human phosphorylated ERK1/2 at Thr202/Tyr204 (clone D13.14.4E; Cell Signaling Technology, Danvers, MA, USA).

Techniques: Expressing, Phospho-proteomics, Co-Culture Assay, Isolation, Injection, Immunohistochemistry, Staining, Control

Journal: Scientific Reports

Article Title: ADSCs stimulated by resistin promote breast cancer cell malignancy via CXCL5 in a breast cancer coculture model

doi: 10.1038/s41598-022-19290-6

Figure Lengend Snippet: Correlation analysis for the protein expression of resistin, CXCL5, and ERK phosphorylation in the tumor and serum specimens from breast cancer patients. ( A ) Representative images of immunohistochemistry (IHC) staining for resistin, CXCL5, and phospho-ERK1/2 expression in breast tumor sections from breast cancer patients. ( B–D ) The quantitative IHC scores were evaluated by HistoQuest software, followed by Pearson correlation (r) analysis between resistin and CXCL5 in ( B ) (n = 96), resistin and phospho-ERK1/2 in ( C ) (n = 45), and CXCL5 and phospho-ERK1/2 in ( D ) (n = 45). ( E ) The serum levels of resistin and CXCL5 in breast cancer patients were determined by ELISA, followed by Pearson correlation (r) analysis (n = 120). The mean ± SD of resistin and CXCL5 was 31.4 ± 15.4 ng/ml and 707.9 ± 293.4 pg/ml, respectively. ( F ) Schematic summary of the current study. Our preclinical and clinical data together suggest that CXCL5 may be secreted by resistin-stimulated ADSCs in the breast tumor microenvironment, promoting breast cancer cell malignancy via the participation of ERK pathway and epithelial-to-mesenchymal transition. The schematic summary in ( F ) was produced using the illustration elements from Servier Medical Art ( https://smart.servier.com ), which is in compliance with the terms of the Creative Commons Attribution 3.0 Unported License ( https://creativecommons.org/licenses/by/3.0/ ).

Article Snippet: The primary antibodies used in this study for IHC are listed as follows: rabbit polyclonal antibody against human Slug (GeneTex, Hsinchu, Taiwan); goat polyclonal antibody against human CXCL5 (R&D Systems, Minneapolis, MN, USA); mouse monoclonal antibody against human resistin (clone C-10; Santa Cruz Biotechnology, Dallas, TX, USA); rabbit monoclonal antibody against human phosphorylated ERK1/2 at Thr202/Tyr204 (clone D13.14.4E; Cell Signaling Technology, Danvers, MA, USA).

Techniques: Expressing, Phospho-proteomics, Immunohistochemistry, Software, Enzyme-linked Immunosorbent Assay, Produced