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: FBXL18 targeted DUSP16 as a ubiquitination substrate. ( A-B ) The results of Co-IP and western blotting assays revealed the endogenous and exogenous 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), DUSP16 (#5523, CST, USA), FLAG (#14793, CST, USA), HA (#3724, CST, USA).

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: FBXL18 promoted EC cell malignancy via DUSP16-mediated activation of JNK signaling. ( A-C ) Western blot analysis of DUSP16, JNK, p-JNK, c-JUN, and p-c-JUN levels in EC cells of siNeg and siDUSP16 groups, and quantitative analysis. ( D-F ) Western blot analysis of DUSP16, JNK, p-JNK, c-JUN, and p-c-JUN levels in EC cells after overexpressing DUSP16, and quantitative analysis. ( G-I ) Western blot analysis of DUSP16, JNK, p-JNK, c-JUN, and p-c-JUN levels in EC cells transfected with LV-Ctrl + Vector, LV-Ctrl + DUSP16, LV-FBXL18 + Vector, LV-FBXL18 + DUSP16, and quantitative analysis. ( J-L ) Western blot analysis of DUSP16, JNK, p-JNK, c-JUN, and p-c-JUN levels in EC cells transfected with shNC + siNeg, shNC + siDUSP16, shFBXL18 + siNeg, shFBXL18 + siDUSP16, and quantitative analysis. * P < 0.05; ** P < 0.01; *** P < 0.001

Article Snippet: The primary antibodies included FBXL18 (sc-100738, Santa Cruz, USA), DUSP16 (#5523, CST, USA), FLAG (#14793, CST, USA), HA (#3724, CST, USA).

Techniques: Activation Assay, Western Blot, Transfection, Plasmid Preparation

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: 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), DUSP16 (#5523, CST, USA), FLAG (#14793, CST, USA), HA (#3724, CST, USA).

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

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: SiRNA specifically targeting DUSP16 or negative control siRNA (siNeg) were obtained from Sangon Biotech (Shanghai, China).

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: SiRNA specifically targeting DUSP16 or negative control siRNA (siNeg) were obtained from Sangon Biotech (Shanghai, China).

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

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: FBXL18 targeted DUSP16 as a ubiquitination substrate. ( A-B ) The results of Co-IP and western blotting assays revealed the endogenous and exogenous 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: SiRNA specifically targeting DUSP16 or negative control siRNA (siNeg) were obtained from Sangon Biotech (Shanghai, China).

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: FBXL18 promoted EC cell malignancy via DUSP16-mediated activation of JNK signaling. ( A-C ) Western blot analysis of DUSP16, JNK, p-JNK, c-JUN, and p-c-JUN levels in EC cells of siNeg and siDUSP16 groups, and quantitative analysis. ( D-F ) Western blot analysis of DUSP16, JNK, p-JNK, c-JUN, and p-c-JUN levels in EC cells after overexpressing DUSP16, and quantitative analysis. ( G-I ) Western blot analysis of DUSP16, JNK, p-JNK, c-JUN, and p-c-JUN levels in EC cells transfected with LV-Ctrl + Vector, LV-Ctrl + DUSP16, LV-FBXL18 + Vector, LV-FBXL18 + DUSP16, and quantitative analysis. ( J-L ) Western blot analysis of DUSP16, JNK, p-JNK, c-JUN, and p-c-JUN levels in EC cells transfected with shNC + siNeg, shNC + siDUSP16, shFBXL18 + siNeg, shFBXL18 + siDUSP16, and quantitative analysis. * P < 0.05; ** P < 0.01; *** P < 0.001

Article Snippet: SiRNA specifically targeting DUSP16 or negative control siRNA (siNeg) were obtained from Sangon Biotech (Shanghai, China).

Techniques: Activation Assay, Western Blot, Transfection, Plasmid Preparation

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: 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: SiRNA specifically targeting DUSP16 or negative control siRNA (siNeg) were obtained from Sangon Biotech (Shanghai, China).

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