mapk pathway sampler kit  (Cell Signaling Technology Inc)

Journal: Scientific Reports

Article Title: Esketamine attenuates bone cancer pain by suppressing MAPK signaling and glial activation in the spinal dorsal horn of rats

doi: 10.1038/s41598-026-38137-y

Figure Lengend Snippet: ESK inhibits MAPK pathway activation in the SDH of BCP rats. ( A–D ) Representative WB images and quantification of phosphorylated JNK ( B ), p38 ( C ), and ERK ( D ) levels. Data are mean ± SEM of biological replicates n = 3. *** P < 0.001 versus sham plus vehicle group, # P < 0.05, ## P < 0.01, ### P < 0.001 versus BCP plus vehicle group, ns, not significant. One-way ANOVA with repeated measures followed by post hoc Tukey test. ( E ) Schematic of experimental timeline showing repeated intrathecal administration of ESK, SB203580 (p38 inhibitor), or SP600125 (JNK inhibitor) on POD 13 to 16. ( F ) Co-treatment with ESK enhanced the MAPK inhibitors induced increase in PWT after intrathecal administration. Notably, co-administration of MAPK inhibitors did not further enhance ESK’s analgesic effect, suggesting that its antinociceptive action mainly involves MAPK pathway inhibition. Data are mean ± SEM of biological replicates n = 7–8 rats/group. Two-way ANOVA with repeated measures followed by post hoc Tukey test. * P < 0.05, ** P < 0.01, *** P < 0.001 vs. BCP + DMSO; # P < 0.05, BCP + ESK+SB203580 vs. BCP + SB203580, BCP + ESK+SP600125 vs. BCP + SP600125 at corresponding time points. ( G ) Western blot of IL-1β, IL-6, and TNF-α expression in the SDH. ( H–J ) Quantification of cytokine levels showed further reductions in IL-1β ( H ), IL-6 ( I ), and TNF-α ( J ) with combined ESK and MAPK inhibitor treatment. Data are mean ± SEM of biological replicates n = 3. * P < 0.05, ** P < 0.01, *** P < 0.001, ns, not significant. One-way ANOVA with repeated measures followed by post hoc Tukey test.

Article Snippet: To assess MAPK pathway involvement, the JNK inhibitor SP600125 (5 μg/10 μl; Cell Signaling Technology, USA) and the p38 inhibitor SB203580 (10 μg/10 μl; Abcam, UK) were dissolved in DMSO to a final DMSO concentration of 1%.

Techniques: Activation Assay, Inhibition, Western Blot, Expressing

Journal: Translational Oncology

Article Title: Zeaxanthin targets TOP2A to regulate autophagy and suppress lung cancer progression via the MAPK/ERK pathway

doi: 10.1016/j.tranon.2025.102658

Figure Lengend Snippet: Zea modulates MAPK/ERK signaling to inhibit LC progression. A: Analysis of gene expression differences pre- and post-Zea treatment; B: Heat map analysis of TOP 50 DEGs; C: GO functional enrichment of differentially expressed genes; D: KEGG pathway enrichment of differentially expressed genes; E: WB analysis of MAPK/ERK pathway proteins. A549 cells: NC, Zea, Zea + Ro 67–7476. F: Cell viability measured by CCK-8; G: Cell proliferation assessed by colony formation; H: Cell migration analyzed by Transwell; I: Cell apoptosis detected by flow cytometry; J: WB of autophagy-related proteins; K: IF analysis of autophagosomes and lysosomes, with LC3 for autophagosomes and LAMP1 for lysosomes. ** P < 0.01, *** P < 0.001. The data is presented as mean ± standard deviation, and inter-group comparisons are conducted using ANOVA and Tukey’s post hoc test.

Article Snippet: We also wondered whether the impact of Zea on LC cells was associated with the MAPK/ERK signaling, so we treated A549 cells with Zea and subsequently added MAPK/ERK pathway activator Ro 67–7476 (MCE, USA) to activate this pathway.

Techniques: Gene Expression, Functional Assay, CCK-8 Assay, Migration, Flow Cytometry, Standard Deviation

Journal: Translational Oncology

Article Title: Zeaxanthin targets TOP2A to regulate autophagy and suppress lung cancer progression via the MAPK/ERK pathway

doi: 10.1016/j.tranon.2025.102658

Figure Lengend Snippet: Zea targets TOP2A to enhance autophagy via the MAPK/ERK pathway and impedes LC progression. A549 cells: oe-NC, oe-TOP2A, A: TOP2A mRNA level detected by qRT-PCR A549 cells: oe-NC, oe-TOP2A, oe-NC + Zea, oe-TOP2A + Zea. B: WB analysis of TOP2A, MAPK/ERK pathway proteins (p-ERK1/2, ERK1/2, p-MEK, MEK), and autophagy-related proteins (LC3-I, LC3-II, Beclin 1); C: IF detection of autophagosome and lysosome formation; D: CCK-8 assay of cell viability; E: Colony formation assay of cell proliferation; F: Transwell assay of cell migration; G: Flow cytometry analysis of cell apoptosis. ** P < 0.01, *** P < 0.001. The data is presented as mean ± standard deviation, and inter-group comparisons are conducted using ANOVA and Tukey’s post hoc test.

Article Snippet: We also wondered whether the impact of Zea on LC cells was associated with the MAPK/ERK signaling, so we treated A549 cells with Zea and subsequently added MAPK/ERK pathway activator Ro 67–7476 (MCE, USA) to activate this pathway.

Techniques: Quantitative RT-PCR, CCK-8 Assay, Colony Assay, Transwell Assay, Migration, Flow Cytometry, Standard Deviation

Journal: Translational Oncology

Article Title: Zeaxanthin targets TOP2A to regulate autophagy and suppress lung cancer progression via the MAPK/ERK pathway

doi: 10.1016/j.tranon.2025.102658

Figure Lengend Snippet: In vivo evidence that Zea targets TOP2A to influence the MAPK/ERK pathway and autophagy to mitigate LC progression. Animal groups: oe-NC, oe-TOP2A, oe-NC + Zea, oe-TOP2A + Zea. A: Tumor images from the mouse model; B: Weight of mouse tumor tissues; C: Volume of mouse tumor tissues; D: HE staining images of mouse tumor tissues; E: IHC detection of TOP2A and KI67 expression levels in tumor tissues; F: WB analysis of MAPK/ERK pathway proteins (p-ERK1/2, ERK1/2, p-MEK, MEK) and autophagy-related proteins (LC3-I, LC3-II, Beclin 1); G: IF detection of autophagosome and lysosome colocalization. *** P < 0.001. The data is presented as mean ± standard deviation, and inter-group comparisons are conducted using ANOVA and Tukey’s post hoc test.

Article Snippet: We also wondered whether the impact of Zea on LC cells was associated with the MAPK/ERK signaling, so we treated A549 cells with Zea and subsequently added MAPK/ERK pathway activator Ro 67–7476 (MCE, USA) to activate this pathway.

Techniques: In Vivo, Staining, Expressing, Standard Deviation