What are the molecular mechanisms that regulate the expression of RNA Polymerase II in cancer?
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The expression of RNA Polymerase II (Pol II) in cancer is regulated by various molecular mechanisms involving key proteins. MYC, a crucial transcription factor in cancer, interacts with Protein Arginine Methyltransferase 5 (PRMT5) to control Pol II termination via dimethylation at R1810, influencing gene expression . Additionally, hairpin Pyrrole-Imidazole (Py-Im) polyamides can induce strong transcriptional arrest by trapping Pol II in a treadmill-like manner, preventing transcription elongation . Furthermore, the tumor suppressor p53 directly interacts with Pol II, altering its conformation to regulate DNA binding and transcription, shedding light on p53-mediated gene expression control . Dysregulation of Pol III isoforms, particularly POLR3G, driven by MYC, impacts the transcription repertoire in cancer, highlighting the role of Pol III identity in transcriptional regulation .
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1 Citations | Not addressed in the paper. |
25 Mar 2021 6 Citations | The tumor suppressor p53's DNA binding domain targets RNA Polymerase II, inducing conformational changes and regulating DNA binding activity, providing insights into p53-regulated gene expression in cancer. |
| Hairpin Py-Im polyamides trap RNA Polymerase II, inducing persistent transcriptional arrest by preventing forward translocation and inducing backtracking, offering insights for developing anti-cancer transcription inhibitors. | |
| MYC interacts with PRMT5 to control RNA Polymerase II methylation (R1810me2s) and termination, influencing gene expression in cancer cells, highlighting a novel regulatory axis in transcriptional control. | |
17 Feb 2022 | MYC interacts with PRMT5 to regulate RNA Polymerase II methylation at R1810, impacting transcription termination. Omomyc inhibits MYC, altering RNAPII distribution and gene expression in cancer cells. |
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