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Fig. 3 | BMC Cancer

Fig. 3

From: A germline mutation of CDKN2A and a novel RPLP1-C19MC fusion detected in a rare melanotic neuroectodermal tumor of infancy: a case report

Fig. 3

Responses of MNTI cell line to epigenetic inhibition and a CDK4/CDK6 inhibitor. MNTI cells were treated with bromodomain inhibitors (a), histone deacetylase inhibitors (b), histone methyltransferase inhibitors (c), lysine demethylase inhibitors (d) or miscellaneous inhibitors (e). Cell viability was reduced in response to a range of small molecule inhibitors of lysine demethylases (d) but was unaffected by inhibitors of other epigenetic mechanisms. Results are normalized to the vehicle control and represent the mean ± s.d. of either 3 biological replicates (day 3, mid gray) or 2 biological replicates (days 7, light gray and 10, dark gray). f Log dose–response curves for CD4/CDK6 inhibitor palbociclib-treated MNTI cells (, magenta) and Ewing sarcoma cell lines: CHP-100 (, purple), A673 (, teal) and SK-N-MC (, orange). Cells were treated with doses of palbociclib or vehicle control (DMSO) for 72 h and those remaining viable were assayed using the MTS reagent. Percentage of viable cells was calculated by normalizing absorbance readings taken at 490 nm. Data are mean ± s.e.m. and representative curves from one of three independent experiments are shown. Inhibitors in (e) targeted: kinases (K00135, 5-iodotubercidin), a methyl-lysine reader (UNC1215), PARP (rucaparabib, olaparib), PHD2 (IOX2), tRNA synthetase (MAZ1392, MAZ1805), DNA methyltransferase (5-aza-deoxy-cytidine, 5-azacitidine) and arginine deiminase (GSK484 low and high doses shown)

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