Fig. 3: Effects of roniciclib on the cell cycle in HONE-1 and HK-1 cells. | Signal Transduction and Targeted Therapy

Fig. 3: Effects of roniciclib on the cell cycle in HONE-1 and HK-1 cells.

From: Pan-CDK inhibition augments cisplatin lethality in nasopharyngeal carcinoma cell lines and xenograft models

Fig. 3

a–b Cell cycle analysis of NPC cell lines treated with roniciclib at two doses at different time points (HONE-1, 40 nM; HK-1, 30 nM; HONE-1, 200 nM; HK-1, 150 nM). Control cells were treated with 0.05% DMSO. Cells were stained immediately with both Annexin V and propidium iodide upon harvesting of cells at the indicated time points and singlet populations were selected via flow cytometry. c Time course and dose-dependent inhibition of direct CDK protein substrates in HONE-1 and HK-1 cells. Roniciclib suppressed the expression of p-NPM at both concentrations by 2 h post treatment, suggesting that CDK1 and CDK2/cyclin E expression may be inhibited, as both CDKs are primary targets of NPM. Expression of p-RNA POL II, MCL-1, and p-Rb was downregulated. Higher doses of roniciclib induced rapid Ser-2 dephosphorylation of the C-terminal domain of RNA polymerase II. Dephosphorylation of RNA pol II downregulated transcription, particularly affecting the levels of mRNAs with short half-lives, such as MCL-1. All experiments were performed in triplicate

Back to article page