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Santa Cruz Biotechnology vcan
<t>VCAN</t> is highly expressed in patients with esophageal cancer. (A) Spearman correlation analysis from TCGA. (B) A total of 13 genes correlated <t>with</t> <t>VEZF1</t> and were associated with cell adhesion functions. (C) Gene levels in patients with esophageal cancer retrieved from the GSE161533 and TCGA database. (D) Kaplan-Meier analysis of VCAN level in normal and cancer stage in ESCC *P<0.05. VCAN, Versican; VEZF1, Vascular Endothelial Zinc Finger 1; TCGA, The Cancer Genome Atlas; FC, Fold Change; PLXNC1, Plexin C1; ERBIN, interacting protein; CLDN, claudin; ARAHGAP, Rho GTPase-activating protein 5; RGMB, Repulsive Guidance Molecule BMP Co-Receptor B; ITGBL, Integrin subunit beta 1; PTPRK, Protein Tyrosine Phosphatase Receptor Type Kappa; DDR, DNA Damage Response; PARD, Par-3 family cell polarity regulator; SPECC1L, sperm antigen with calponin homology and coiled-coil domains 1 like; CDON, Cell Adhesion Associated, Oncogene Regulated; PTPRT, protein tyrosine phosphatase, receptor type, T.
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Images

1) Product Images from "Visfatin facilitates esophageal cancer migration by suppressing miR-3613-5p expression and promoting VEZF1/VCAN production"

Article Title: Visfatin facilitates esophageal cancer migration by suppressing miR-3613-5p expression and promoting VEZF1/VCAN production

Journal: Oncology Reports

doi: 10.3892/or.2025.8961

VCAN is highly expressed in patients with esophageal cancer. (A) Spearman correlation analysis from TCGA. (B) A total of 13 genes correlated with VEZF1 and were associated with cell adhesion functions. (C) Gene levels in patients with esophageal cancer retrieved from the GSE161533 and TCGA database. (D) Kaplan-Meier analysis of VCAN level in normal and cancer stage in ESCC *P<0.05. VCAN, Versican; VEZF1, Vascular Endothelial Zinc Finger 1; TCGA, The Cancer Genome Atlas; FC, Fold Change; PLXNC1, Plexin C1; ERBIN, interacting protein; CLDN, claudin; ARAHGAP, Rho GTPase-activating protein 5; RGMB, Repulsive Guidance Molecule BMP Co-Receptor B; ITGBL, Integrin subunit beta 1; PTPRK, Protein Tyrosine Phosphatase Receptor Type Kappa; DDR, DNA Damage Response; PARD, Par-3 family cell polarity regulator; SPECC1L, sperm antigen with calponin homology and coiled-coil domains 1 like; CDON, Cell Adhesion Associated, Oncogene Regulated; PTPRT, protein tyrosine phosphatase, receptor type, T.
Figure Legend Snippet: VCAN is highly expressed in patients with esophageal cancer. (A) Spearman correlation analysis from TCGA. (B) A total of 13 genes correlated with VEZF1 and were associated with cell adhesion functions. (C) Gene levels in patients with esophageal cancer retrieved from the GSE161533 and TCGA database. (D) Kaplan-Meier analysis of VCAN level in normal and cancer stage in ESCC *P<0.05. VCAN, Versican; VEZF1, Vascular Endothelial Zinc Finger 1; TCGA, The Cancer Genome Atlas; FC, Fold Change; PLXNC1, Plexin C1; ERBIN, interacting protein; CLDN, claudin; ARAHGAP, Rho GTPase-activating protein 5; RGMB, Repulsive Guidance Molecule BMP Co-Receptor B; ITGBL, Integrin subunit beta 1; PTPRK, Protein Tyrosine Phosphatase Receptor Type Kappa; DDR, DNA Damage Response; PARD, Par-3 family cell polarity regulator; SPECC1L, sperm antigen with calponin homology and coiled-coil domains 1 like; CDON, Cell Adhesion Associated, Oncogene Regulated; PTPRT, protein tyrosine phosphatase, receptor type, T.

Techniques Used:

VCAN is involved in visfatin-induced esophageal cancer migration. Cells were stimulated with visfatin and VCAN expression was examined using (A) RT-qPCR and (B) western blot analysis. (C) VCAN siRNA transfection efficiency confirmed by western blot analysis. (D) KYSE410 cells were transfected with or without VCAN siRNA followed by visfatin treatment and cell (E) migration and (F) invasion were examined. (G) CE81T cells were transfected with VCAN siRNA and treated with visfatin; cell (H) migration and (I) invasion were examined. Cells were transfected with miR-3613-5p mimic or VEZF-1 siRNA and treated with visfatin; VCAN expression was examined using (J) RT-qPCR and (K) western blotting. (L) KYSE 410 cells treated with PI3K (Ly294002), AKT and mTOR (rapamycin) inhibitors and visfatin treatment to assess effects on (M) migration and (N) invasion. (O) CE81T cells treated with PI3K (Ly294002), AKT and mTOR (rapamycin) inhibitors and visfatin treatment were assayed for (P) cell migration and (Q) invasion. Gene Expression Omnibus dataset GSE77861 shows significantly increased mRNA expression of (R) NAMPT, (S) miR-3613-5p, (T) VEZF1 and (U) VCAN in esophageal cancer compared with normal tissue. *P<0.05 vs. control; # P<0.05 vs. visfatin. miR, microRNA; VCAN, versican; RT-q, Reverse Transcriptase Quantitative; si, small interfering; VEZf-1, Vascular Endothelial Zinc Finger 1; NAMPT, Nicotinamide phosphoribosyltransferase; Akti, Akt inhibitor.
Figure Legend Snippet: VCAN is involved in visfatin-induced esophageal cancer migration. Cells were stimulated with visfatin and VCAN expression was examined using (A) RT-qPCR and (B) western blot analysis. (C) VCAN siRNA transfection efficiency confirmed by western blot analysis. (D) KYSE410 cells were transfected with or without VCAN siRNA followed by visfatin treatment and cell (E) migration and (F) invasion were examined. (G) CE81T cells were transfected with VCAN siRNA and treated with visfatin; cell (H) migration and (I) invasion were examined. Cells were transfected with miR-3613-5p mimic or VEZF-1 siRNA and treated with visfatin; VCAN expression was examined using (J) RT-qPCR and (K) western blotting. (L) KYSE 410 cells treated with PI3K (Ly294002), AKT and mTOR (rapamycin) inhibitors and visfatin treatment to assess effects on (M) migration and (N) invasion. (O) CE81T cells treated with PI3K (Ly294002), AKT and mTOR (rapamycin) inhibitors and visfatin treatment were assayed for (P) cell migration and (Q) invasion. Gene Expression Omnibus dataset GSE77861 shows significantly increased mRNA expression of (R) NAMPT, (S) miR-3613-5p, (T) VEZF1 and (U) VCAN in esophageal cancer compared with normal tissue. *P<0.05 vs. control; # P<0.05 vs. visfatin. miR, microRNA; VCAN, versican; RT-q, Reverse Transcriptase Quantitative; si, small interfering; VEZf-1, Vascular Endothelial Zinc Finger 1; NAMPT, Nicotinamide phosphoribosyltransferase; Akti, Akt inhibitor.

Techniques Used: Migration, Expressing, Quantitative RT-PCR, Western Blot, Transfection, Gene Expression, Control, Reverse Transcription

Mechanisms underlying the roles of visfatin in esophageal cancer cell migration and invasion. Visfatin enhances cell migration and invasion in esophageal cancer cells. The inhibition of miR-3613-5p and the promotion of the VEZF1/VCAN axis mediate visfatin-induced esophageal cancer cell motility. miR, microRNA; VEZF1, Vascular Endothelial Zinc Finger 1; VCAN, Versican; UTR, Untranslated region.
Figure Legend Snippet: Mechanisms underlying the roles of visfatin in esophageal cancer cell migration and invasion. Visfatin enhances cell migration and invasion in esophageal cancer cells. The inhibition of miR-3613-5p and the promotion of the VEZF1/VCAN axis mediate visfatin-induced esophageal cancer cell motility. miR, microRNA; VEZF1, Vascular Endothelial Zinc Finger 1; VCAN, Versican; UTR, Untranslated region.

Techniques Used: Migration, Inhibition



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Image Search Results


Graphical summary of the study In the Discovery phase, a 4-protein biomarker panel (THBS1, NID1, PTX3, and VCAN) was discovered by proteomic analysis of sEVs derived from an isogenic HBEC model using mass spectrometry. The biomarker panel was tested in sEVs isolated from 22 cancer cell lines by ELISA. In the Validation phase, a cohort consisting of 250 healthy individuals and 514 patients with multiple cancers was recruited to assess the performance of the biomarker panel. Plasma/serum sEVs were isolated and analyzed by ELISA. In the Translation phase, a multiplex microfluidic device incorporating SERS was developed for simultaneous profiling of the 4-protein biomarker panel in a lung cancer screening setting. The expression levels of 4 proteins are reflected by the Raman intensities of the corresponding Raman reporters.

Journal: Cell Reports Medicine

Article Title: Early-stage multi-cancer detection through a plasma extracellular vesicle protein signature

doi: 10.1016/j.xcrm.2026.102694

Figure Lengend Snippet: Graphical summary of the study In the Discovery phase, a 4-protein biomarker panel (THBS1, NID1, PTX3, and VCAN) was discovered by proteomic analysis of sEVs derived from an isogenic HBEC model using mass spectrometry. The biomarker panel was tested in sEVs isolated from 22 cancer cell lines by ELISA. In the Validation phase, a cohort consisting of 250 healthy individuals and 514 patients with multiple cancers was recruited to assess the performance of the biomarker panel. Plasma/serum sEVs were isolated and analyzed by ELISA. In the Translation phase, a multiplex microfluidic device incorporating SERS was developed for simultaneous profiling of the 4-protein biomarker panel in a lung cancer screening setting. The expression levels of 4 proteins are reflected by the Raman intensities of the corresponding Raman reporters.

Article Snippet: Human VCAN ELISA Kit , Novus Biologicals , Cat# NBP2-75353.

Techniques: Biomarker Discovery, Derivative Assay, Mass Spectrometry, Isolation, Enzyme-linked Immunosorbent Assay, Clinical Proteomics, Multiplex Assay, Expressing

Transformation-induced changes to the protein composition of cell-derived sEVs (A) The morphology of isolated sEVs was assessed using transmission electron microscopy. Images of normal and transformed HBEC-derived sEVs (scale bars, 200 nm). (B) Nanoparticle analysis using tunable resistive pulse sensing of sEVs isolated from HBECs demonstrates that the majority of sEVs have a size range between 30 and 150 nm, and that transformation does not result in an increase in sEV secretion. (C) Western blot of sEVs from HBECs demonstrating the presence of sEV proteins HSP70 and CD63 and the absence of the cell marker calnexin. (D) Label-free mass spectrometry identified 148 proteins with greater abundance in sEVs derived from transformed HBECs (FDR <0.02), of which 15 were annotated as extracellular proteins. (E) Mass spectrometry results were confirmed using ELISA for THBS1, NID1, PTX3, and VCAN in sEVs derived from normal and transformed HBECs. (F) sEVs derived from 22 cancer cell lines including NSCLC (SKMES1, H1650, HCC4006, and H2170), glioblastoma ([GBM], D54, D270, U87, and U118), colorectal cancer ([CRC], HT29 and SW620), breast cancer ([BCa], BT549, MDA231, and MDA436), prostate cancer ([PCa], PC3 and LNCaP), melanoma ([MEL], A375, MAMEL65, and SKMEL28), esophageal cancer ([ECa], OE19), and ovarian cancer ([OVA], A2780, CAOV3, IGROV1, and OVCAR8) showed a clear increase in expression of THBS1, NID1, PTX3, and VCAN in relation to the average levels of sEVs from normal cells ([HBEC] 30KT, HOSE 6.3, and HOSE 17.1). Samples in mass spectrometry and ELISA were measured in triplicate. See also and .

Journal: Cell Reports Medicine

Article Title: Early-stage multi-cancer detection through a plasma extracellular vesicle protein signature

doi: 10.1016/j.xcrm.2026.102694

Figure Lengend Snippet: Transformation-induced changes to the protein composition of cell-derived sEVs (A) The morphology of isolated sEVs was assessed using transmission electron microscopy. Images of normal and transformed HBEC-derived sEVs (scale bars, 200 nm). (B) Nanoparticle analysis using tunable resistive pulse sensing of sEVs isolated from HBECs demonstrates that the majority of sEVs have a size range between 30 and 150 nm, and that transformation does not result in an increase in sEV secretion. (C) Western blot of sEVs from HBECs demonstrating the presence of sEV proteins HSP70 and CD63 and the absence of the cell marker calnexin. (D) Label-free mass spectrometry identified 148 proteins with greater abundance in sEVs derived from transformed HBECs (FDR <0.02), of which 15 were annotated as extracellular proteins. (E) Mass spectrometry results were confirmed using ELISA for THBS1, NID1, PTX3, and VCAN in sEVs derived from normal and transformed HBECs. (F) sEVs derived from 22 cancer cell lines including NSCLC (SKMES1, H1650, HCC4006, and H2170), glioblastoma ([GBM], D54, D270, U87, and U118), colorectal cancer ([CRC], HT29 and SW620), breast cancer ([BCa], BT549, MDA231, and MDA436), prostate cancer ([PCa], PC3 and LNCaP), melanoma ([MEL], A375, MAMEL65, and SKMEL28), esophageal cancer ([ECa], OE19), and ovarian cancer ([OVA], A2780, CAOV3, IGROV1, and OVCAR8) showed a clear increase in expression of THBS1, NID1, PTX3, and VCAN in relation to the average levels of sEVs from normal cells ([HBEC] 30KT, HOSE 6.3, and HOSE 17.1). Samples in mass spectrometry and ELISA were measured in triplicate. See also and .

Article Snippet: Human VCAN ELISA Kit , Novus Biologicals , Cat# NBP2-75353.

Techniques: Transformation Assay, Derivative Assay, Isolation, Transmission Assay, Electron Microscopy, Tunable Resistive Pulse Sensing, Western Blot, Marker, Mass Spectrometry, Enzyme-linked Immunosorbent Assay, Expressing

The transformed sEV signature accurately diagnoses cancer in patient plasma (A) The expression levels of THBS1, NID1, PTX3, and VCAN in plasma derived from cancer patients are increased in comparison to healthy controls. Samples were measured in triplicate. Lines in dot plots represent median values. (B) ROC curves of classification of each cancer type compared to healthy controls demonstrate excellent diagnostic capability of the 4-protein sEV biomarker panel with an AUC of 0.91–1. (C) The sensitivity of the diagnostic sEV signature for each cancer type was evaluated at a fixed specificity of 90%, 95%, and 99%. Error bars represent 95% confidence intervals. Healthy ( n = 250), NSCLC ( n = 139), glioblastoma ([GBM], n = 57), colorectal cancer ([CRC], n = 42), prostate cancer ([PCa], n = 30), melanoma ([MEL], n = 100), gastric cancer ([GCa], n = 19), esophageal cancer ([ECa], n = 98), small cell lung cancer ([SCLC], n = 29). See also and .

Journal: Cell Reports Medicine

Article Title: Early-stage multi-cancer detection through a plasma extracellular vesicle protein signature

doi: 10.1016/j.xcrm.2026.102694

Figure Lengend Snippet: The transformed sEV signature accurately diagnoses cancer in patient plasma (A) The expression levels of THBS1, NID1, PTX3, and VCAN in plasma derived from cancer patients are increased in comparison to healthy controls. Samples were measured in triplicate. Lines in dot plots represent median values. (B) ROC curves of classification of each cancer type compared to healthy controls demonstrate excellent diagnostic capability of the 4-protein sEV biomarker panel with an AUC of 0.91–1. (C) The sensitivity of the diagnostic sEV signature for each cancer type was evaluated at a fixed specificity of 90%, 95%, and 99%. Error bars represent 95% confidence intervals. Healthy ( n = 250), NSCLC ( n = 139), glioblastoma ([GBM], n = 57), colorectal cancer ([CRC], n = 42), prostate cancer ([PCa], n = 30), melanoma ([MEL], n = 100), gastric cancer ([GCa], n = 19), esophageal cancer ([ECa], n = 98), small cell lung cancer ([SCLC], n = 29). See also and .

Article Snippet: Human VCAN ELISA Kit , Novus Biologicals , Cat# NBP2-75353.

Techniques: Transformation Assay, Clinical Proteomics, Expressing, Derivative Assay, Comparison, Diagnostic Assay, Biomarker Discovery

Evaluation of a multiplex microfluidic device applicable for liquid biopsy testing in a cancer screening setting (A) Clinical follow-up by CT imaging of 2 representative benign patients B1 and B2. Red arrows indicated nodules in patients’ lungs. B1 had a granuloma-cryptococcal infection, and the lesion was found less dense after 26 months. B2 had a lesion in the vicinity of emphysema, which resolved after 21 months. (B) Schematic of multiplex microfluidic device consisting of a pair of asymmetric circular electrodes. Electrodes are conjugated with an anti-THBS1 antibody to capture cancer-derived sEVs. SERS nanotags carrying designated Raman reporters and paired target antibodies (against THBS1, NID1, PTX3, and VCAN) are used for labeling captured sEVs and then analyzed by SERS mapping. (C) Representative false-color SERS spectral images demonstrating an enrichment of THBS1, NID1, PTX3, and VCAN in early-stage NSCLC patients (M1 and M2) compared to patients with benign diseases (B1 and B2). Scale bars, 10 μm. (D) The Raman intensity of each biomarker THBS1, NID1, PTX3, and VCAN in benign ( n = 27) and early-stage NSCLC ( n = 41) patients. a.u., arbitrary units. Samples were measured in triplicate. Lines in dot plots represent median values. (E) ROC curve of logistic regression classification indicating an AUC of 0.85 in detecting early-stage NSCLC cases compared to benign cases in a cancer screening setting. (F) The confusion matrix of the multiplex microfluidic device. See also and and .

Journal: Cell Reports Medicine

Article Title: Early-stage multi-cancer detection through a plasma extracellular vesicle protein signature

doi: 10.1016/j.xcrm.2026.102694

Figure Lengend Snippet: Evaluation of a multiplex microfluidic device applicable for liquid biopsy testing in a cancer screening setting (A) Clinical follow-up by CT imaging of 2 representative benign patients B1 and B2. Red arrows indicated nodules in patients’ lungs. B1 had a granuloma-cryptococcal infection, and the lesion was found less dense after 26 months. B2 had a lesion in the vicinity of emphysema, which resolved after 21 months. (B) Schematic of multiplex microfluidic device consisting of a pair of asymmetric circular electrodes. Electrodes are conjugated with an anti-THBS1 antibody to capture cancer-derived sEVs. SERS nanotags carrying designated Raman reporters and paired target antibodies (against THBS1, NID1, PTX3, and VCAN) are used for labeling captured sEVs and then analyzed by SERS mapping. (C) Representative false-color SERS spectral images demonstrating an enrichment of THBS1, NID1, PTX3, and VCAN in early-stage NSCLC patients (M1 and M2) compared to patients with benign diseases (B1 and B2). Scale bars, 10 μm. (D) The Raman intensity of each biomarker THBS1, NID1, PTX3, and VCAN in benign ( n = 27) and early-stage NSCLC ( n = 41) patients. a.u., arbitrary units. Samples were measured in triplicate. Lines in dot plots represent median values. (E) ROC curve of logistic regression classification indicating an AUC of 0.85 in detecting early-stage NSCLC cases compared to benign cases in a cancer screening setting. (F) The confusion matrix of the multiplex microfluidic device. See also and and .

Article Snippet: Human VCAN ELISA Kit , Novus Biologicals , Cat# NBP2-75353.

Techniques: Multiplex Assay, Imaging, Infection, Derivative Assay, Labeling, Biomarker Discovery

Evaluation of the multiplex microfluidic device in a longitudinally monitored cohort of pre- and post-surgery NSCLC patients (A) Representative false-color SERS spectral images demonstrating a decrease of THBS1, NID1, PTX3, and VCAN in post-surgery NSCLC patients (P2 post and P12 post) compared to paired pre-surgery (P2 pre and P12 pre) patients. Scale bars, 10 μm. (B) Heatmap showing the log 2 fold changes in Raman intensities of THBS1, NID1, PTX3, and VCAN in post-surgery NSCLC patients ( n = 12), relative to their paired pre-surgery samples. Samples were measured in triplicate. Negative values (blue) indicate decreased expression after surgery, while positive values (red) indicate increased expression. See also .

Journal: Cell Reports Medicine

Article Title: Early-stage multi-cancer detection through a plasma extracellular vesicle protein signature

doi: 10.1016/j.xcrm.2026.102694

Figure Lengend Snippet: Evaluation of the multiplex microfluidic device in a longitudinally monitored cohort of pre- and post-surgery NSCLC patients (A) Representative false-color SERS spectral images demonstrating a decrease of THBS1, NID1, PTX3, and VCAN in post-surgery NSCLC patients (P2 post and P12 post) compared to paired pre-surgery (P2 pre and P12 pre) patients. Scale bars, 10 μm. (B) Heatmap showing the log 2 fold changes in Raman intensities of THBS1, NID1, PTX3, and VCAN in post-surgery NSCLC patients ( n = 12), relative to their paired pre-surgery samples. Samples were measured in triplicate. Negative values (blue) indicate decreased expression after surgery, while positive values (red) indicate increased expression. See also .

Article Snippet: Human VCAN ELISA Kit , Novus Biologicals , Cat# NBP2-75353.

Techniques: Multiplex Assay, Expressing

VCAN is highly expressed in patients with esophageal cancer. (A) Spearman correlation analysis from TCGA. (B) A total of 13 genes correlated with VEZF1 and were associated with cell adhesion functions. (C) Gene levels in patients with esophageal cancer retrieved from the GSE161533 and TCGA database. (D) Kaplan-Meier analysis of VCAN level in normal and cancer stage in ESCC *P<0.05. VCAN, Versican; VEZF1, Vascular Endothelial Zinc Finger 1; TCGA, The Cancer Genome Atlas; FC, Fold Change; PLXNC1, Plexin C1; ERBIN, interacting protein; CLDN, claudin; ARAHGAP, Rho GTPase-activating protein 5; RGMB, Repulsive Guidance Molecule BMP Co-Receptor B; ITGBL, Integrin subunit beta 1; PTPRK, Protein Tyrosine Phosphatase Receptor Type Kappa; DDR, DNA Damage Response; PARD, Par-3 family cell polarity regulator; SPECC1L, sperm antigen with calponin homology and coiled-coil domains 1 like; CDON, Cell Adhesion Associated, Oncogene Regulated; PTPRT, protein tyrosine phosphatase, receptor type, T.

Journal: Oncology Reports

Article Title: Visfatin facilitates esophageal cancer migration by suppressing miR-3613-5p expression and promoting VEZF1/VCAN production

doi: 10.3892/or.2025.8961

Figure Lengend Snippet: VCAN is highly expressed in patients with esophageal cancer. (A) Spearman correlation analysis from TCGA. (B) A total of 13 genes correlated with VEZF1 and were associated with cell adhesion functions. (C) Gene levels in patients with esophageal cancer retrieved from the GSE161533 and TCGA database. (D) Kaplan-Meier analysis of VCAN level in normal and cancer stage in ESCC *P<0.05. VCAN, Versican; VEZF1, Vascular Endothelial Zinc Finger 1; TCGA, The Cancer Genome Atlas; FC, Fold Change; PLXNC1, Plexin C1; ERBIN, interacting protein; CLDN, claudin; ARAHGAP, Rho GTPase-activating protein 5; RGMB, Repulsive Guidance Molecule BMP Co-Receptor B; ITGBL, Integrin subunit beta 1; PTPRK, Protein Tyrosine Phosphatase Receptor Type Kappa; DDR, DNA Damage Response; PARD, Par-3 family cell polarity regulator; SPECC1L, sperm antigen with calponin homology and coiled-coil domains 1 like; CDON, Cell Adhesion Associated, Oncogene Regulated; PTPRT, protein tyrosine phosphatase, receptor type, T.

Article Snippet: The small interfering (si)RNAs targeting VEZF1 (cat no. sc-94046) and VCAN (cat no. sc-41903) were purchased from Santa Cruz Biotechnology, Inc. A non-targeting negative control siRNA (cat no. D-001810-10-05) was purchased from Thermo Fisher Scientific, Inc. PI3K (Ly294002) inhibitor (cat. no. ALX-270-038) was obtained from Enzo Life Sciences, Inc. AKT (cat. no. A6730) and mTOR (rapamycin) inhibitors (cat. no. R0395) were obtained from Sigma-Aldrich (Merck KGaA).

Techniques:

VCAN is involved in visfatin-induced esophageal cancer migration. Cells were stimulated with visfatin and VCAN expression was examined using (A) RT-qPCR and (B) western blot analysis. (C) VCAN siRNA transfection efficiency confirmed by western blot analysis. (D) KYSE410 cells were transfected with or without VCAN siRNA followed by visfatin treatment and cell (E) migration and (F) invasion were examined. (G) CE81T cells were transfected with VCAN siRNA and treated with visfatin; cell (H) migration and (I) invasion were examined. Cells were transfected with miR-3613-5p mimic or VEZF-1 siRNA and treated with visfatin; VCAN expression was examined using (J) RT-qPCR and (K) western blotting. (L) KYSE 410 cells treated with PI3K (Ly294002), AKT and mTOR (rapamycin) inhibitors and visfatin treatment to assess effects on (M) migration and (N) invasion. (O) CE81T cells treated with PI3K (Ly294002), AKT and mTOR (rapamycin) inhibitors and visfatin treatment were assayed for (P) cell migration and (Q) invasion. Gene Expression Omnibus dataset GSE77861 shows significantly increased mRNA expression of (R) NAMPT, (S) miR-3613-5p, (T) VEZF1 and (U) VCAN in esophageal cancer compared with normal tissue. *P<0.05 vs. control; # P<0.05 vs. visfatin. miR, microRNA; VCAN, versican; RT-q, Reverse Transcriptase Quantitative; si, small interfering; VEZf-1, Vascular Endothelial Zinc Finger 1; NAMPT, Nicotinamide phosphoribosyltransferase; Akti, Akt inhibitor.

Journal: Oncology Reports

Article Title: Visfatin facilitates esophageal cancer migration by suppressing miR-3613-5p expression and promoting VEZF1/VCAN production

doi: 10.3892/or.2025.8961

Figure Lengend Snippet: VCAN is involved in visfatin-induced esophageal cancer migration. Cells were stimulated with visfatin and VCAN expression was examined using (A) RT-qPCR and (B) western blot analysis. (C) VCAN siRNA transfection efficiency confirmed by western blot analysis. (D) KYSE410 cells were transfected with or without VCAN siRNA followed by visfatin treatment and cell (E) migration and (F) invasion were examined. (G) CE81T cells were transfected with VCAN siRNA and treated with visfatin; cell (H) migration and (I) invasion were examined. Cells were transfected with miR-3613-5p mimic or VEZF-1 siRNA and treated with visfatin; VCAN expression was examined using (J) RT-qPCR and (K) western blotting. (L) KYSE 410 cells treated with PI3K (Ly294002), AKT and mTOR (rapamycin) inhibitors and visfatin treatment to assess effects on (M) migration and (N) invasion. (O) CE81T cells treated with PI3K (Ly294002), AKT and mTOR (rapamycin) inhibitors and visfatin treatment were assayed for (P) cell migration and (Q) invasion. Gene Expression Omnibus dataset GSE77861 shows significantly increased mRNA expression of (R) NAMPT, (S) miR-3613-5p, (T) VEZF1 and (U) VCAN in esophageal cancer compared with normal tissue. *P<0.05 vs. control; # P<0.05 vs. visfatin. miR, microRNA; VCAN, versican; RT-q, Reverse Transcriptase Quantitative; si, small interfering; VEZf-1, Vascular Endothelial Zinc Finger 1; NAMPT, Nicotinamide phosphoribosyltransferase; Akti, Akt inhibitor.

Article Snippet: The small interfering (si)RNAs targeting VEZF1 (cat no. sc-94046) and VCAN (cat no. sc-41903) were purchased from Santa Cruz Biotechnology, Inc. A non-targeting negative control siRNA (cat no. D-001810-10-05) was purchased from Thermo Fisher Scientific, Inc. PI3K (Ly294002) inhibitor (cat. no. ALX-270-038) was obtained from Enzo Life Sciences, Inc. AKT (cat. no. A6730) and mTOR (rapamycin) inhibitors (cat. no. R0395) were obtained from Sigma-Aldrich (Merck KGaA).

Techniques: Migration, Expressing, Quantitative RT-PCR, Western Blot, Transfection, Gene Expression, Control, Reverse Transcription

Mechanisms underlying the roles of visfatin in esophageal cancer cell migration and invasion. Visfatin enhances cell migration and invasion in esophageal cancer cells. The inhibition of miR-3613-5p and the promotion of the VEZF1/VCAN axis mediate visfatin-induced esophageal cancer cell motility. miR, microRNA; VEZF1, Vascular Endothelial Zinc Finger 1; VCAN, Versican; UTR, Untranslated region.

Journal: Oncology Reports

Article Title: Visfatin facilitates esophageal cancer migration by suppressing miR-3613-5p expression and promoting VEZF1/VCAN production

doi: 10.3892/or.2025.8961

Figure Lengend Snippet: Mechanisms underlying the roles of visfatin in esophageal cancer cell migration and invasion. Visfatin enhances cell migration and invasion in esophageal cancer cells. The inhibition of miR-3613-5p and the promotion of the VEZF1/VCAN axis mediate visfatin-induced esophageal cancer cell motility. miR, microRNA; VEZF1, Vascular Endothelial Zinc Finger 1; VCAN, Versican; UTR, Untranslated region.

Article Snippet: The small interfering (si)RNAs targeting VEZF1 (cat no. sc-94046) and VCAN (cat no. sc-41903) were purchased from Santa Cruz Biotechnology, Inc. A non-targeting negative control siRNA (cat no. D-001810-10-05) was purchased from Thermo Fisher Scientific, Inc. PI3K (Ly294002) inhibitor (cat. no. ALX-270-038) was obtained from Enzo Life Sciences, Inc. AKT (cat. no. A6730) and mTOR (rapamycin) inhibitors (cat. no. R0395) were obtained from Sigma-Aldrich (Merck KGaA).

Techniques: Migration, Inhibition