fk228 romidepsin  (MedChemExpress)

Journal: Communications Biology

Article Title: EPI-SauriCas9-based mouse ovarian cancer models recapitulating pten deletion in patients

doi: 10.1038/s42003-025-09437-2

Figure Lengend Snippet: A Schematic overview of the compound library screening strategy, showing the range of epigenetic and natural compounds tested. B Comparative drug sensitivity analysis of MEPP versus PREPP cells, identifying compounds preferentially targeting the Trp53 / Pten -deficient background. C Identification and validation of FK228 and thioguanine as ovarian cancer–selective therapeutic candidates, supported by screening across multiple human ovarian cancer cell lines. D Experimental design for in vivo drug testing: MEPP cells were implanted subcutaneously and treated intraperitoneally with vehicle, FK228, or thioguanine (top). Representative images of tumors at necropsy are shown (bottom). E , F Tumor growth inhibition by FK228 and thioguanine ( n = 8 biologically independent animals). E Tumor growth curves in each treatment group (mean ± s.e.m.). F Tumor weights at autopsy; data analyzed by one-way ANOVA with Dunnett’s multiple comparisons test. G H&E and Ki67 IHC staining of tumors treated with vehicle, FK228, or thioguanine. Scale bar, 50 μm. H TUNEL assay of tumors treated with vehicle, FK228, or thioguanine. Scale bar, 50 μm. I , J Quantification of Ki67 scores ( n = 8 biologically independent samples) ( I ) and TUNEL-positive cells ( n = 4 biologically independent biological samples) ( J ) in vehicle-, FK228-, and thioguanine-treated tumors. Data are shown in mean ± s.e.m. Statistical significance determined by one-way ANOVA with Dunnett’s multiple comparisons test. K Gene set enrichment analysis (GSEA) of MEPP tumors treated with FK228 or thioguanine using Reactome, Gene Ontology, and Hallmark gene sets. Only pathways with FDR q < 0.05 are shown; representative pathways are labeled. L Viability of PO1 organoids following 72 h exposure to FK228 or thioguanine, analyzed by one-way ANOVA with Dunnett’s multiple comparisons test ( n = 5 independent viability experiments).

Article Snippet: FK228 (1 mg kg −1 ; MCE, Cat# HY-15149), thioguanine (1.5 mg kg −1 ; MCE, Cat# HY-13765) or vehicle were administered intraperitoneally twice a week once tumors reached 50–100 mm3.

Techniques: Drug discovery, Biomarker Discovery, In Vivo, Inhibition, Immunohistochemistry, TUNEL Assay, Labeling

Journal: Cancer Medicine

Article Title: Prognostic and Monitoring Utility of Serum CEA in Lung Adenocarcinoma: Differential Roles in EGFR‐TKI and Chemotherapy Treatments

doi: 10.1002/cam4.71170

Figure Lengend Snippet: CEACAM5 expression plasticity is regulated by EGFR‐TKI selection and mediated by epigenetic and cytokine stimulation. (A) Gene expression profiling analysis evaluating CEACAM5, CDH1, and VIM expression in EGFR‐TKI sensitive HCC827 versus resistant counterpart HCC827ER1 (ER1) and HCC827ER2 (ER2) cells from the GSE38310 database. * p < 0.05; *** p < 0.001. (B) Gene expression profiling analysis evaluating CEACAM5 , the epithelial marker gene CLDN1 , and the mesenchymal marker gene CDH2 and VIM expression in EGFR‐TKI sensitive primary tumor cells (MGH119) versus resistant (MGH119GR) cells from the GSE64322 database. (C) qRT‐PCR analysis assessing CEACAM5 , CDH1 , and VIM expression in HCC827 cells treated with or without romidepsin (HDACi, 1 nM) for 3 weeks. qRT‐PCR analysis evaluating CEACAM5 , CDH1 , and VIM expression in HCC827 cells treated with or without TGF‐β (1 ng/mL) for 3 weeks. qRT‐PCR analysis evaluating CEACAM5 , CDH1 , and VIM expression in A549 treated with or without TGF‐β (1 ng/mL) for 3 weeks. * p < 0.05; ** p < 0.01; *** p < 0.001.

Article Snippet: Romidepsin (FK228) was obtained from Med Chem Express (Monmouth Junction, NJ, USA).

Techniques: Expressing, Selection, Gene Expression, Marker, Quantitative RT-PCR

Journal: Science Advances

Article Title: Temporal regulation of gene expression through integration of p53 dynamics and modifications

doi: 10.1126/sciadv.adp2229

Figure Lengend Snippet: ( A ) Phosphorylations or acetylations at the indicated residues of p53 were monitored by Western blots of total cell lysates (left) or of p53 immunoprecipitates (IP) (right) in the first and second pulses. Loading was normalized for total p53. Modifications indicated in red showed differences in levels between the two pulses. ( B ) Quantification of the Western blot from A, normalized to total p53 levels ( n = 3 biological replicates, error bars indicate SD). ( C ) Western blot of acetylation at lysine-373 (K373-Ac) or lysine-382 (K382-Ac) of p53 at the indicated time points after 10-Gy x-ray irradiation. Actin is shown as a loading control. ( D ) Quantification of time-course Western blot signal from (B), normalized to the maximum level attained for each species over the time course ( n = 3 biological replicates, error bars indicate SD). ( E ) Schematic of experiment showing addition of inhibitor(s) at the trough between p53 peaks (4.5 hours post irradiation). ( F ) Western blot of p53 acetylated at K373, K381, or K382 in the presence or absence of HDACi or SIRTi added at the time point shown in A. Total p53 is shown as a loading control. ( G ) Left: BTG2 mRNA levels following 48-hour knockdown with control or BTG2 short interfering (si)RNA. Right: Western blot of p53 acetylated at K373 or K382 following siRNA silencing of BTG2 (see Materials and Methods) and after the indicated number of hours after irradiation.

Article Snippet: Romidepsin/Depsipeptide (HDACi) (Adooq Bioscience, FK228) and Sirtinol (SIRTi) (Sigma-Aldrich, 566320) were added at 10 nM, and 50 μM, respectively.

Techniques: Western Blot, Irradiation, Control, Knockdown

Journal: Science Advances

Article Title: Temporal regulation of gene expression through integration of p53 dynamics and modifications

doi: 10.1126/sciadv.adp2229

Figure Lengend Snippet: ( A ) qPCR analysis of the mRNA levels of the indicated genes at 8 hours after irradiation treated with or without HDACi, normalized to mRNA levels in unirradiated cells. Error bars represent SD from three biological replicates. * P < 0.05, ** P < 0.01 by t test. ( B ) Schematic of p53 constructs harboring single or double K➔R mutations. ( C ) qPCR analysis of mRNA levels of CDKN1A , PAI1 , PML , and PUMA after the second p53 pulse in cells expressing the indicated p53 variants and treated with or without HDACi. Error bars represent SD from three biological replicates. * P < 0.05, ** P < 0.01 by t test (all conditions compared to WT + HDACi).

Article Snippet: Romidepsin/Depsipeptide (HDACi) (Adooq Bioscience, FK228) and Sirtinol (SIRTi) (Sigma-Aldrich, 566320) were added at 10 nM, and 50 μM, respectively.

Techniques: Irradiation, Construct, Expressing