es 2  (MedChemExpress)

Journal: Molecular Systems Biology

Article Title: Spatial proteomics of ovarian cancer precursors delineates early disease changes and drug targets

doi: 10.1038/s44320-025-00168-4

Figure Lengend Snippet: ( A ) Experimental workflow describing cholesterol biosynthesis inhibitor (AY9944 or simvastatin) treatment of ovarian cancer lines in combination with carboplatin. Cancer cells were treated for 72 h with AY9944 or simvastatin in combination with carboplatin. Cell viability was measured by MTT assay and normalized to untreated controls. Drug synergy was evaluated by Highest Single Agent (HSA) method, where synergy value >10 indicates synergistic effect, −10 to 10 indicates additive or no interaction, <−10 indicates antagonistic effect. ( B ) Cell viability assay of ovarian cancer cell lines (OAW-42, OVCAR-8, ES-2, and EFO-21) treated with different doses of carboplatin, the DHCR7 inhibitor AY9944 and simvastatin. Treatment effect relative to matched vehicle. Experiments were performed in biological triplicates (with n = 3 technical replicates each). Mean ± SD; significance test: unpaired Student’s t -test: ns (not significant), ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001. Exact p values are provided in the Appendix Table . ( C ) Synergy score map of OVCAR-8, EFO-21, ES-2, and OAW-42 cells treated with different concentrations of carboplatin and the DHCR7 inhibitor AY9944. The mean HSA (Highest Single Agent) score for OVCAR-8, EFO-21, ES-2, and OAW-42 was 14.9 ( p value = 5.13e − 10 ), 13.5 ( p value = 3.30e-09), 7.52 ( p value = 2.05e-3), 2.38 ( p value = 2.86e-01) synergy value >10 indicates a synergistic effect, −10 to 10 indicates an additive or no interaction, and <−10 indicates an antagonistic effect.

Article Snippet: For OAW-42, OVCAR-8, and ES-2, we plated 4000 cells/well, and for EFO-21, we plated 6000 cells/well and we cultured the cells in full growth medium for 24 h. The medium was then removed and replaced with new full medium containing different concentrations of AY-9944 (MedChemExpress, #HY-107420), carboplatin (Merck, #C2538) or combinations of the two drugs.

Techniques: MTT Assay, Viability Assay

Journal: Molecular Systems Biology

Article Title: Spatial proteomics of ovarian cancer precursors delineates early disease changes and drug targets

doi: 10.1038/s44320-025-00168-4

Figure Lengend Snippet: ( A – H ) Dose–response curves (top left: AY9944 or simvastatin; bottom left: carboplatin) and dose–response matrices (right) for ES-2 ( A , B ), EFO-21 ( C , D ), OVCAR-8 ( E , F ), and OAW-42 ( G , H ) cells treated with AY9944 and carboplatin or simvastatin and carboplatin, respectively, alone or in combination. Experiments were performed in biological sextuplicate, each with n = 3 technical replicates.

Article Snippet: For OAW-42, OVCAR-8, and ES-2, we plated 4000 cells/well, and for EFO-21, we plated 6000 cells/well and we cultured the cells in full growth medium for 24 h. The medium was then removed and replaced with new full medium containing different concentrations of AY-9944 (MedChemExpress, #HY-107420), carboplatin (Merck, #C2538) or combinations of the two drugs.

Techniques:

Journal: Oncology Research

Article Title: 3 β -Hydroxysterol Δ 24-Reductase Promotes Ovarian Cancer Progression by Activating the TGF- β 1/Smad2/3 Signaling Pathway

doi: 10.32604/or.2025.065451

Figure Lengend Snippet: DHCR24 promotes OC cell proliferation. ( a ) Transfection efficiency of DHCR24-shRNA in SKOV3 cells, detected using qPCR; ( b ) Left: WB results verified the establishment of an in vitro model showing stable and low expression of DHCR24. Right: Corresponding quantitative analysis results; ( c ) Transfection efficiency of overexpressed DHCR24 in ES2 cells, detected using qPCR; ( d ) Left: Establishment of an in vitro model showing stable overexpression of DHCR24, verified using WB. Right: Corresponding quantitative analysis results; ( e ) CCK-8 test showing that DHCR24 overexpression promotes OC cell proliferation (3 × 10 3 cells/well); ( f ) Left: Colony formation assay showing that overexpression of DHCR24 promotes OC cell proliferation. Right: Corresponding quantitative analysis results (4 × 10 2 cells/well); ( g ) CCK-8 test showing that DHCR24 knockdown inhibits OC cell proliferation (3 × 10 3 cells/well); ( h ) Left: Colony formation assay showing that DHCR24 knockdown inhibits the proliferation of OC cells. Right: Corresponding quantitative analysis results (4 × 10 2 cells/well). All experiments were independently repeated three times. Note: DHCR24, 3β-hydroxysterol Δ24-reductase; OC, ovarian cancer; qPCR, quantitative PCR; WB, western blot; CCK-8, cell counting kit-8. ns, no significance; ** p < 0.01, *** p < 0.001

Article Snippet: SKOV3 and ES2 cells were treated with the DHCR24 inhibitor SH-42 (Cat. No. HY-143228, MCE, NJ, USA).

Techniques: Transfection, shRNA, In Vitro, Expressing, Over Expression, CCK-8 Assay, Colony Assay, Knockdown, Real-time Polymerase Chain Reaction, Western Blot, Cell Counting

Journal: Oncology Research

Article Title: 3 β -Hydroxysterol Δ 24-Reductase Promotes Ovarian Cancer Progression by Activating the TGF- β 1/Smad2/3 Signaling Pathway

doi: 10.32604/or.2025.065451

Figure Lengend Snippet: DHCR24 promotes migration, invasion, and EMT of OC cells. ( a ) Left: Transwell experiment results showing that DHCR24 knockdown inhibits OC cell migration and invasion. Right: Corresponding quantitative analysis results (SKOV3: 2 × 10 4 cells/well); ( b ) Left: Transwell experiment results showing that DHCR24 overexpression promotes migration and invasion of OC cells. Right: Corresponding quantitative analysis results (ES2: 2 × 10 4 cells/well); ( c ) Left: Wound healing experiment results showing that DHCR24 knockdown inhibits the migration of OC cells. Right: Corresponding quantitative analysis results; ( d ) Left: Changes in EMT-related proteins in OC cells before and after DHCR24 knockdown, detected using WB. Right: Corresponding quantitative analysis results; ( e ) Left: Changes in EMT-related proteins in OC cells before and after DHCR24 overexpression, detected using WB. Right: Corresponding quantitative analysis results. All experiments were independently repeated three times. Note: DHCR24, 3β-hydroxysterol Δ24-reductase; OC, ovarian cancer; EMT, Epithelial-mesenchymal transition; WB, western blot. ns, no significance; ** p < 0.01, *** p < 0.001

Article Snippet: SKOV3 and ES2 cells were treated with the DHCR24 inhibitor SH-42 (Cat. No. HY-143228, MCE, NJ, USA).

Techniques: Migration, Knockdown, Over Expression, Western Blot

Journal: Oncology Research

Article Title: 3 β -Hydroxysterol Δ 24-Reductase Promotes Ovarian Cancer Progression by Activating the TGF- β 1/Smad2/3 Signaling Pathway

doi: 10.32604/or.2025.065451

Figure Lengend Snippet: SH-42 suppressed the proliferative, migration, and invasion capabilities of OC cells. ( a ) CCK-8 assay showing the effect of SH-42 on the proliferative ability of SKOV3 cells (3 × 10 3 cells/well); ( b ) Transwell assay showing the effect of SH-42 on the migration and invasion of SKOV3 cells (2 × 10 4 cells/well); ( c ) CCK-8 assay showing the effects of DHCR24 overexpression and SH-42 on the proliferation of ES2 cells (3 × 10 3 cells/well); ( d ) Transwell assay showing the effects of DHCR24 overexpression and SH-42 on the migration and invasion of ES2 cells (2 × 10 4 cells/well). All experiments were independently repeated three times. Note: CCK-8, cell counting kit-8; DHCR24, 3β-hydroxysterol Δ24-reductase; ns, no significance; ** p < 0.01, *** p < 0.001

Article Snippet: SKOV3 and ES2 cells were treated with the DHCR24 inhibitor SH-42 (Cat. No. HY-143228, MCE, NJ, USA).

Techniques: Migration, CCK-8 Assay, Transwell Assay, Over Expression, Cell Counting