p erk  (Proteintech)

Journal: iScience

Article Title: Uncovering cantharidin’s mechanism for cholangiocarcinoma treatment using patient-derived tumor organoids

doi: 10.1016/j.isci.2025.114136

Figure Lengend Snippet: Cantharidin induces apoptosis and inhibits proliferation by downregulating p-ERK1/2–c-Fos signaling pathway (A) Western blot (WB) analysis and corresponding quantification (B) of p-ERK1/2, apoptosis-related proteins (Bax and Bcl-xL), a marker of cell cycle progression (Cyclin D1), and endoplasmic reticulum stress response markers (GRP78 and CHOP). ( n = 3). (C and D) Quantification (C) of p-ERK1/2 staining and representative IF images (D) ( n = 10). (E) WB analysis and quantification of p-ERK1/2 and c-Fos ( n = 3). (F) WB analysis and quantification of Bax, Bcl-Xl, Cyclin D1, GRP78, and CHOP ( n = 3). Con, control; Can, cantharidin; Can+Ro, Cantharidin+Ro67-7476. Data are presented as mean ± SD. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, and ∗∗∗∗ p < 0.0001, ns: no significant difference. t test was used to compare between two groups. One-way ANOVA was used to compare between three groups.

Article Snippet: The PDOs were treated with 200 nM p -ERK agonist Ro 67–7476 (MedChemExpress, China) for 6 h before cantharidin treatment to activate the p -ERK signaling pathway.

Techniques: Western Blot, Marker, Staining, Control

Journal: iScience

Article Title: Uncovering cantharidin’s mechanism for cholangiocarcinoma treatment using patient-derived tumor organoids

doi: 10.1016/j.isci.2025.114136

Figure Lengend Snippet: Cantharidin exerts antitumor effects by downregulating the p-ERK1/2-c-Fos signaling pathway in PDOXs (A) Intratumoral concentrations of cantharidin in PDOX5 and PDOX7 models following a single oral administration at a dose of 1 mg/kg ( n = 5). (B) Schematic of the pharmacodynamic experiments. (C) Representative image, growth curves, and tumor weight of PDOX5 after administration for 4 weeks ( n = 5). (D) Expression levels and corresponding quantification (E) of p-ERK1/2 and c-Fos of PDOX5 after administration for 4 weeks ( n = 3). (F) Representative Ki67 and TUNEL staining images of PDOX5 with different treatments and quantitative analysis of Ki67 + and TUNEL + cells ( n = 10). (G) Representative image, growth curves, and tumor weight of PDOX7 after administration for 4 weeks ( n = 5). (H) Expression levels and corresponding quantification (I) of p-ERK1/2 and c-Fos of PDOX7 after administration for 4 weeks ( n = 3). (J) Representative Ki67 and TUNEL staining images of PDOX7 with different treatments and quantitative analysis of Ki67 + and TUNEL + cells ( n = 10). Con, control; Can, cantharidin; Can+Ro, Cantharidin+Ro67-7476. The data are presented as mean ± SD. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001. One-way ANOVA was used to compare between different groups.

Article Snippet: The PDOs were treated with 200 nM p -ERK agonist Ro 67–7476 (MedChemExpress, China) for 6 h before cantharidin treatment to activate the p -ERK signaling pathway.

Techniques: Expressing, TUNEL Assay, Staining, Control

Journal: iScience

Article Title: Uncovering cantharidin’s mechanism for cholangiocarcinoma treatment using patient-derived tumor organoids

doi: 10.1016/j.isci.2025.114136

Figure Lengend Snippet: Mechanism diagram: cantharidin exerts antitumor effects by downregulating the p-ERK1/2-c-Fos signaling pathway.

Article Snippet: The PDOs were treated with 200 nM p -ERK agonist Ro 67–7476 (MedChemExpress, China) for 6 h before cantharidin treatment to activate the p -ERK signaling pathway.

Techniques: