TL;DR
This Review examines how transcriptional or co-transcriptional processes become dysregulated in cancer cells, and how this dysfunction might create targetable vulnerabilities, and summarizes advances in therapeutic strategies targeting transcriptional CDKs.
Cyclins and cyclin‐dependent kinases (CDKs) are frequently dysregulated in human cancers and represent compelling therapeutic targets. Beyond their well‐recognized roles in cell cycle control, CDK/cyclin complexes orchestrate diverse oncogenic processes, including transcription, genome maintenance, epigenetics, metabol...
The molecular functions of the CDK9/positive transcription elongation factor b (P-TEFb) axis, its role in super-enhancer-driven oncogenic programs, and the mechanisms by which CDK9 inhibition promotes apoptosis, epigenetic derepression, and tumor microenvironment remodeling are summarized.
Transcriptional cyclin-dependent kinases (tCDKs) are master regulators of gene expression, controlling RNAPII activity and RNA synthesis across multiple phases of the transcription cycle. While highly controlled transcription is essential for all cellular processes and functions, aberrant gene expression or corrupted a...
Global upregulation of transcription, or hypertranscription, is observed in most human cancers, driven by the action of oncogene-encoded transcription factors (TFs). TF interactions with RNA Polymerase II (Pol II) are mediated by kinases that phosphorylate the Pol II C-terminal domain (CTD) to drive productive elonga...
Cyclin-dependent kinase 9 (CDK9) inhibition represents a promising therapeutic strategy in cancers that disrupts RNA polymerase II pause release and collapses oncogenic transcripts. Here, we show that CDK9 inhibition also induces widespread transposable element (TE) activation across diverse cancer types. In acute myel...
This work highlights non-canonical transcriptional kinases that could operate alongside and beyond CDKs to modulate transcription by RNAPII, and discusses how these kinases could introduce context-specific CTD modifications that enable transcriptional plasticity, facilitate rapid loci-specific activation, and integrate...
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