Inducing apoptosis in cancer cells is a critical therapeutic strategy that selectively eliminates malignant cells and inhibits tumor progression without inducing inflammation. The application of meriolins has demonstrated their capacity to function as pan-specific kinase inhibitors, predominantly targeting CDKs, thereby inducing apoptosis. Studies indicate that these substances block the cell cycle and trigger apoptotic signaling pathways, resulting in a substantial decrease in cell growth and survival of leukemia cells.

The mechanisms underlying this apoptosis induction are analyzed in greater detail using specific CDK inhibitors of the cell cycle and transcription. The present study investigated the cell-cycle inhibitory potential, transcription influence, RNA polymerase inhibition, and transcription-factor modulation of diverse CDK inhibitors.

We could demonstrate that the inhibition of transcription, especially through CDK9, is particularly cytotoxic in leukemia cells. We could further show that by targeting CDK9, RNA polymerase II is hindered from its function, consequently preventing the transcription of anti-apoptotic proteins such as Mcl-1. This disruption in the equilibrium between pro- and anti-apoptotic proteins results in programmed cell death.

These findings highlight the therapeutic potential of CDK9 inhibition as a targeted strategy to effectively induce apoptosis in leukemia cells over transcriptional inhibition.