Journal: Journal of cellular physiology

Article Title: Mitogen-Dependent Regulation of DUSP1 Governs ERK and p38 Signaling During Early 3T3-L1 Adipocyte Differentiation

doi: 10.1002/jcp.25248

Figure Lengend Snippet: DUSP and inflammatory genes analyzed in this study

Article Snippet: For adipocytes, these stimuli include insulin and the synthetic glucocorticoid dexamethasone ( Kusari et al., 1997 ; Kassel et al., 2001 ). table ft1 table-wrap mode="anchored" t5 caption a7 Symbol Name/alias Accession ABI number C T Dual specificity phosphatases GP MKB NLS NES EJP Dusp1 MKP-1,hVH1 I ● ● NM_013642 Mm00457274_g1 24 Dusp2 PAC-1 I ● ● NM_010090 Mm00839675_g1 30 Dusp4 MKP-2, hVH2 I ● ● NM_176933 Mm00723761_m1 25 Dusp5 hVH3 I ● ● NM_001085390 Mm01266104_m1 27 Dusp6 MKP-3, rVH6 II ● ● E NM_026268 Mm00650255_g1 24 Dusp7 MKP-X II ● ● E NM_153459 Mm00463228_m1 27 Dusp9 MKP-4 II ● ● E NM_029352 Mm00512646_m1 27 Dusp8 M3/6, hVH5 III ● ● ● J/P NM_008748 Mm00456230_m1 27 Dusp10 MKP-5 III ● J/P NM_022019 Mm00517678_m1 24 Dusp16 MKP-7, MKP-M III ● ● ● J/P NM_130447 Mm00459935_m1 25 Inflammatory genes IL-6 Interleukin-6 NM_031168 Mm99999064_m1 32 TNFα Tumor necrosis factor-alpha NM_013693 Mm99999068_m1 28 Reference gene 18S 18 Ribosomal RNA X03205 4342930E 9 Open in a separate window DUSP group (GP), MAPK binding domain (MKB), nuclear localization sequence (NLS), nuclear export sequence (NES), ERK (E), JNK (J), p38 (P), threshold cycle (C T ) measured in lean adipose tissue.

Techniques:

Journal: Cancer cell international

Article Title: FBXL18 promotes endometrial carcinoma progression via destabilizing DUSP16 and thus activating JNK signaling pathway.

doi: 10.1186/s12935-025-03808-9

Figure Lengend Snippet: Fig. 5 FBXL18 targeted DUSP16 as a ubiquitination substrate. (A-B) The results of Co-IP and western blotting assays revealed the endogenous and exog enous interaction of FBXL18 and DUSP16. (C-D) qRT-PCR analysis of DUSP16 mRNA levels after silencing or overexpressing FBXL18 in KLE and Ishikawa cells. (E-F) Western blot analysis of DUSP16 protein level in EC cells of shNC and shFBXL18 groups, and quantitative analysis. (G-H) Western blot analysis of DUSP16 protein level in EC cells after overexpressing FBXL18, and quantitative analysis. (I-J) DUSP16 protein half-life in EC cells of LV-Control and LV- FBXL18 groups were evaluated by CHX chase assay. (K-L) Comparison of DUSP16 protein half-life in EC cells stably knockdown of FBXL18 and control cells. (M-N) The ubiquitination status of endogenous DUSP16 after silencing or overexpressing FBXL18 in EC cells were determined by immunoprecipitation and western blotting. *P < 0.05; **P < 0.01; ***P < 0.001

Article Snippet: The primary antibodies included FBXL18 (sc-100738, Santa Cruz, USA; 1:500), DUSP16 (#5523, CST, USA; 1:1000), GAPDH (GB15004100, Servicebio, China; 1:500), JNK (#9252, CST, USA; 1:1000), p-JNK (#9251, CST, USA; 1:500), c-Jun (#9165, CST, USA; 1:1000), and p-c-Jun (#3270, CST, USA; 1:1000).

Techniques: Ubiquitin Proteomics, Co-Immunoprecipitation Assay, Western Blot, Quantitative RT-PCR, Control, Comparison, Stable Transfection, Knockdown, Immunoprecipitation

Journal: Cancer cell international

Article Title: FBXL18 promotes endometrial carcinoma progression via destabilizing DUSP16 and thus activating JNK signaling pathway.

doi: 10.1186/s12935-025-03808-9

Figure Lengend Snippet: Fig. 7 Silence of FBXL18 inhibited EC growth in vivo. (A) Tumor volumes of shNC and shFBXL18 groups were determined at different defined time points. (B) Representative images of xenograft tumors in shNC and shFBXL18 groups. (C) Tumor weights of shNC and shFBXL18 groups were measured at the end point. (E) Western blot analysis of FBXL18, DUSP16, JNK, p-JNK, c-JUN, p-c-JUN, and EMT-related markers in tumor samples of shNC and shFBXL18 groups, and quantitative analysis. (F) qRT-PCR analysis of FBXL18 and DUSP16 in tumor samples of shNC and shFBXL18 groups. *P < 0.05; **P < 0.01; ***P < 0.001

Article Snippet: The primary antibodies included FBXL18 (sc-100738, Santa Cruz, USA; 1:500), DUSP16 (#5523, CST, USA; 1:1000), GAPDH (GB15004100, Servicebio, China; 1:500), JNK (#9252, CST, USA; 1:1000), p-JNK (#9251, CST, USA; 1:500), c-Jun (#9165, CST, USA; 1:1000), and p-c-Jun (#3270, CST, USA; 1:1000).

Techniques: In Vivo, Western Blot, Quantitative RT-PCR

Journal: Cancer Cell International

Article Title: Exosomal transfer of miR-769-5p promotes osteosarcoma proliferation and metastasis by targeting DUSP16

doi: 10.1186/s12935-021-02257-4

Figure Lengend Snippet: DUSP16 is down-regulated in OS and is a downstream target gene of miR-769-5p. A Bioinformatics analysis showed that hsa-miR-769-5p has a total of 14 target genes in miRDB, miRTarBase, and TargetScan; B, C The mRNA expression level of DUSP16 in OS cell lines and hFOB1.19 ( B ) and clinical samples ( C ); D , E The protein level of DUSP16 in OS cell lines and hFOB1.19 ( D ) and clinical samples ( E ); F Representative immunohistochemical staining of DUSP16 between OS tissues and adjacent tissues; G Negative correlation between miR-769-5p and DUSP16 expression in OS tissues; H Luciferase reporter assay was performed to confirm that miR-769-5p directly bound to the 3′-UTR region of DUSP16. Luciferase activity was analyzed in OS cells co-transfected with miR-769-5p mimics or negative control with pGL3-DUSP16-WT or pGL3- DUSP16-MUT; I , J The expression of DUSP16 in OS cells after alteration of miR-769-5p expression was detected by qRT-PCR ( I ) and western blot ( J ); K , L Western blot ( K ) and immunohistochemical analysis ( L ) were performed to evaluate DUSP16 expression in vivo; n = 5 mice/group. Data are presented as the means ± SD. *P < 0.05, **P < 0.01, ***P < 0.001

Article Snippet: GenScript (Nanjing, China) synthesized wild-type DUSP16 (WT-DUSP16-3 UTR) and mutant DUSP16 (MUT-DUSP16-3 UTR).

Techniques: Expressing, Immunohistochemical staining, Staining, Luciferase, Reporter Assay, Activity Assay, Transfection, Negative Control, Quantitative RT-PCR, Western Blot, In Vivo

Journal: Cancer Cell International

Article Title: Exosomal transfer of miR-769-5p promotes osteosarcoma proliferation and metastasis by targeting DUSP16

doi: 10.1186/s12935-021-02257-4

Figure Lengend Snippet: miR-769-5p promotes EMT and proliferation by suppressing DUSP16 in OS cells. A Western blot analysis was conducted to evaluate the EMT-related protein levels. Rescue experiments for miR-769-5p mimics were conducted via the ectopic expression of DUSP16 in MG63 cells. Rescue experiments for miR-769-5p inhibitor were conducted by downregulating DUSP16 in 143B cells; B-F Rescue experiments were conducted using the Scratch assay ( B , D ), transwell migration assay ( C , E ) and transwell invasion assay ( C , F ); G Western blot analysis was also conducted to evaluate the cell-cycle-related proteins level; H–K Rescue experiments were also conducted using the EdU assay ( H , I ), clone formation assay ( H , J ) and CCK-8 assay ( K ). Data are presented as the means ± SD. *P < 0.05, **P < 0.01, ***P < 0.001

Article Snippet: GenScript (Nanjing, China) synthesized wild-type DUSP16 (WT-DUSP16-3 UTR) and mutant DUSP16 (MUT-DUSP16-3 UTR).

Techniques: Western Blot, Expressing, Wound Healing Assay, Transwell Migration Assay, Transwell Invasion Assay, EdU Assay, Tube Formation Assay, CCK-8 Assay

Journal: Cancer Cell International

Article Title: Exosomal transfer of miR-769-5p promotes osteosarcoma proliferation and metastasis by targeting DUSP16

doi: 10.1186/s12935-021-02257-4

Figure Lengend Snippet: miR-769-5p regulates the JNK/p38 MAPK signaling pathway by targeting DUSP16. A Representative images of western blot analysis of p-JNK, JNK, p-ERK, ERK, p-P38, P38 and DUSP16 levels in transfected MG63 and 143B cells; B Representative images of western blot analysis of p-JNK, JNK, N-cadherin, Vimentin, E-cadherin, c-Myc, CDK4 and cyclin D1 levels in transfected MG63 and 143B cells treated with the JNK inhibitor sp600125 and the JNK activator Anisomycin, respectively

Article Snippet: GenScript (Nanjing, China) synthesized wild-type DUSP16 (WT-DUSP16-3 UTR) and mutant DUSP16 (MUT-DUSP16-3 UTR).

Techniques: Western Blot, Transfection

Journal: Cancer Cell International

Article Title: Exosomal transfer of miR-769-5p promotes osteosarcoma proliferation and metastasis by targeting DUSP16

doi: 10.1186/s12935-021-02257-4

Figure Lengend Snippet: BMSC-derived exosomes can be taken up by OS cells. A Transmission electron micrograph of exosomes derived from BSMCs; B Nanoparticle tracking analysis of the diameter and concentration of exosomes; C Exosomal biomarkers protein were further examined by western blot; D Uptake of Dil-labelled exosomes by MG63 and 143B cells was detected; E , F The mRNA expression level of miR-769-5p ( E ) and DUSP16 ( F ) was detected by qRT-PCR in different groups; G The expression of DUSP16 protein was detected by western blotting in different groups. Data are presented as the means ± SD. *P < 0.05, **P < 0.01, ***P < 0.001

Article Snippet: GenScript (Nanjing, China) synthesized wild-type DUSP16 (WT-DUSP16-3 UTR) and mutant DUSP16 (MUT-DUSP16-3 UTR).

Techniques: Derivative Assay, Transmission Assay, Concentration Assay, Western Blot, Expressing, Quantitative RT-PCR

Journal: Cancer Cell International

Article Title: Exosomal transfer of miR-769-5p promotes osteosarcoma proliferation and metastasis by targeting DUSP16

doi: 10.1186/s12935-021-02257-4

Figure Lengend Snippet: Identification of Exosomes in the Serum of Patients and Graphical Abstract. A Transmission electron micrographs of exosomes derived from OS patients and healthy volunteers; B The expression of miR-769-5p in serum exosomal of OS patients compared to volunteers; C miR-769-5p derived from BMSCs exosomes promotes OS cells migration, invasion and proliferation by downregulating DUSP16 and then activating the JNK/P38 MAPK signaling pathway. Data are presented as the means ± SD. *P < 0.05, **P < 0.01, ***P < 0.001

Article Snippet: GenScript (Nanjing, China) synthesized wild-type DUSP16 (WT-DUSP16-3 UTR) and mutant DUSP16 (MUT-DUSP16-3 UTR).

Techniques: Transmission Assay, Derivative Assay, Expressing, Migration