epigenetic inhibitors  (TargetMol)

Journal: Experimental & Molecular Medicine

Article Title: DNA methyltransferase inhibition is a therapeutic vulnerability in VHL-deficient renal cell carcinoma cells

doi: 10.1038/s12276-026-01663-w

Figure Lengend Snippet: a Stable overexpression of VHL-HA plasmid in 786-O cells (a VHL mutated RCC cell). Western blotting detected the protein level of VHL, HA tag and its downstream target genes HIF-2α in this VHL-isogenic 786-O cell pair. Data are shown as the mean ± s.d., n = 3. b A schematic diagram of synthetic lethal drug screen using VHL-isogenic 786-O cell pair on the Epigenetics Compound Library. c Selectivity index (fold-difference in IC 50 values between VHL −/− and wtVHL OE cells) plot to identify top five synthetic lethal drug candidates. d–g Dose–response curve of 786-O VHL-isogenic cell pair ( d ) and VHL non-isogenic cell pair ( f ) treated with decitabine for 72 h. Data are shown as the mean ± s.d., n = 3. The representative images of cell density with the indicated concentration of decitabine for wtVHL OE and VHL −/− ( e ) and Caki-1 and 769-p ( g ) cells. h , i Azacitidine effect on cell viability in 786-O VHL-isogenic cell pair ( h ) and VHL non-isogenic cell pair ( i ). Data are shown as the mean ± s.d., n = 3. ** P < 0.01, *** P < 0.001 between two indicated groups, Student’s t -test. j , k Dose–response curve of 786-O VHL-isogenic cell pair treated with RC-3117 ( j ) and SGI-1027 ( k ). Data are shown as the mean ± s.d., n = 3. l Chemical structures of DNMT inhibitors used in this study. m–p Western blotting detected the protein level of VHL in H1975 ( m ) and PLC/PRF/5 cells ( o ) and decitabine effect on cell viability of VHL-depleted H1975 cells ( n ) and PLC/PRF/5 ( p ). Data are shown as the mean ± s.d., n = 3. ** P < 0.01, **** P < 0.001 between two indicated groups, Student’s t -test.

Article Snippet: Epigenetics compounds library contains 138 small molecules which was purchased from Selleck Chemicals.

Techniques: Over Expression, Plasmid Preparation, Western Blot, Drug discovery, Concentration Assay

Journal: Neuro-Oncology Advances

Article Title: Epigenetic buffering of proteotoxic stress by EHMT2 enables meningioma growth

doi: 10.1093/noajnl/vdag037

Figure Lengend Snippet: EHMT2/G9a inhibition decreases meningioma growth in vivo. (A) Light micrograph of a tissue section stained with hematoxylin and eosin showing the growth of human CH-157MN meningioma cells in the subdural space of a mouse after intracranial transplantation. Note the mass effect of the meningioma on the underlying brain (arrows). Scale Bar in A: 1 mm. (B) Schematic of treatment regimen for in vivo meningioma growth experiment illustrated in panels C and D . Created in BioRender. Berry (2026) https://BioRender.com/bwz1g0s . (C) Luciferase bioluminescence imaging of intracranial EGFP-Firefly Luciferase-CH-157MN human meningioma cells. Triplicate images of the same mice obtained at day 7 post implantation and day 13 post implantation after daily treatment with UNC0631 (20 mg/kg i.p.) or vehicle control. (D) Data shown is the luminescence in millions of photons/second as a measure of tumor size after daily i.p. administration of UNC0631 or vehicle. * P < .05. (E) Summary diagram illustrating the role of epigenetic buffering of proteotoxic stress by EHMT2/G9a in meningioma cell survival. Created in BioRender. Berry, B. (2026) https://BioRender.com/mli57fn .

Article Snippet: The CH-157MN established human meningioma cell line was plated at a density of approximately 2000 cells/well in 384-well culture dishes for 24 h. The cells were then exposed in triplicate for 48 h to compounds obtained from the Library of Pharmacologically Active Compounds (LO1280, Sigma) at a concentration of 10 μM, a kinase inhibitor library (L1200, SelleckChem) at a concentration of 2 μM, or an epigenetics compound library (L1900, SelleckChem) at a concentration of 2 μM.

Techniques: Inhibition, In Vivo, Staining, Transplantation Assay, Luciferase, Imaging, Control