Journal: European Journal of Histochemistry : EJH

Article Title: Overexpression of GPER1 suppressed esophageal carcinoma growth via activating cAMP pathway

doi: 10.4081/ejh.2026.4422

Figure Lengend Snippet: Inhibition of the cAMP/PKA pathway attenuates GPER1-induced ferroptosis in esophageal cancer cells. KYSE70 and KYSE150 cells were treated with or without the cAMP/PKA inhibitor H89 (10 μM) for 24 h under four conditions: negative control with vehicle (NC + Veh), negative control with H89 (NC + H89), GPER1 overexpression with vehicle (GPER1-OE + Veh), and GPER1 overexpression with H89 (GPER1-OE + H89). a,d ) Cell viability was determined by CCK-8 assay in KYSE70 ( a ) and KYSE150 ( d ) cells. b,e ) Intracellular ROS levels were measured by flow cytometry using a DCFH-DA probe in KYSE70 ( b ) and KYSE150 ( e ) cells. c,f ) Intracellular Fe²⁺ content was quantified by an iron assay kit in KYSE70 ( c ) and KYSE150 ( f ) cells. g ) Protein expression levels of the ferroptosis markers ACSL4 and GPX4, and the cAMP pathway components p-CREB1 and CREB1, were analyzed by Western blotting in both KYSE70 and KYSE150 cells; left panels show representative Western blot images, and the right panels show the corresponding quantitative densitometric analysis of the protein bands, normalized to GAPDH (for ACSL4 and GPX4) or total CREB1 (for p-CREB1). All quantitative data are presented as the mean ±SD from three independent experiments (n=3). Statistical significance was determined by one-way ANOVA followed by Tukey's post-hoc test; * p <0.05, ** p <0.01, *** p <0.001, **** p <0.0001; ns, not significant.

Article Snippet: To functionally validate the role of the cAMP pathway in GPER1-induced ferroptosis, KYSE70 and KYSE150 cells with or without GPER1 overexpression were treated with the cAMP/PKA pathway inhibitor H89 (MedChemExpress, Monmouth Junction, NJ, USA).

Techniques: Inhibition, Negative Control, Over Expression, CCK-8 Assay, Flow Cytometry, Iron Assay, Expressing, Western Blot

Journal: Poultry Science

Article Title: 17β-estradiol mediates sex-biased progesterone receptor expression via estrogen receptor α in chicken pituitary

doi: 10.1016/j.psj.2025.106210

Figure Lengend Snippet: Effects of E 2 -BSA (2 nM, 3 h) on PGR mRNA level in female chick pituitary cells in the presence of distinct pharmacological drugs, including U73 (PLC inhibitor, 3 μM), 2-APB (IP3R antagonist, 10 μM), AEB (pan-PKC inhibitor, 10 μM), GSK (MEK1/2 inhibitor, 10 μM), LY (ERK1/2 inhibitor, 10 μM), NIL (calcium channel blocker, 3 μM), JNK8 (JNK1/2/3 inhibitor, 2 μM), GW (p38 MAPK inhibitor, 10 μM), ZSTK (PI3K inhibitor, 10 μM), MK (AKT1/2/3 inhibitor, 2 μM), MDL (AC inhibitor, 10 μM) and H89 (PKA inhibitor, 1 μM). The expression level of PGR was normalized by β-actin and expressed as the fold change compared with control group (without drug treatment). Statistical analyses were performed using one-way ANOVA followed by Dunnett’s test, each value represents the mean ± SEM of four replicates (n = 4). Exact p-values are shown for significant comparisons, ‘ns’ indicates no statistical significance (p>0.05).

Article Snippet: Pharmacological drugs targeting the components of signaling pathways, including ZSTK474 (ZSTK, Cat#S1072), MK-2206 dihydrochloride (MK, Cat#S1078), GSK1120212 (GSK, Cat#S2673), LY3214996 (LY, Cat#S8534), H89 2HCl (H89, Cat#S1582), nilvadipine (NIL, Cat#2721), U-73122 (U73, Cat#S8011), AEB071 (AEB, Cat#S2791), losmapimod (GW, Cat#S7215), MDL-12330A (MDL, Cat#E6418), and 2-aminoethoxydiphenyl borate (2-APB, Cat#S6657), were obtained from Selleck Chemicals (Houston, US), while JNK-IN-8 (JNK8, Cat#HY-13319) was supplied by TargetMol.

Techniques: Expressing, Control