AI Article Synopsis
- Comprehensive genomic studies identify key mutations in cancer progression, but the related transcriptional changes are often unclear due to analysis biases.
- A new comprehensive prostate cancer transcriptome atlas has been created, offering insights into the qualitative and quantitative aspects of tumor progression, revealing that most cancers follow a similar trajectory marked by specific biological changes.
- Using advanced models and single-cell analysis, researchers show that tumor progression is driven by transcriptional adaptation rather than existing cancer cell populations, with EZH2 identified as a crucial gene influencing this process; a web resource is available for further exploration of these transcriptional changes.
Article Abstract
Comprehensive genomic studies have delineated key driver mutations linked to disease progression for most cancers. However, corresponding transcriptional changes remain largely elusive because of the bias associated with cross-study analysis. Here, we overcome these hurdles and generate a comprehensive prostate cancer transcriptome atlas that describes the roadmap to tumor progression in a qualitative and quantitative manner. Most cancers follow a uniform trajectory characterized by upregulation of polycomb-repressive-complex-2, G2-M checkpoints, and M2 macrophage polarization. Using patient-derived xenograft models, we functionally validate our observations and add single-cell resolution. Thereby, we show that tumor progression occurs through transcriptional adaption rather than a selection of pre-existing cancer cell clusters. Moreover, we determine at the single-cell level how inhibition of EZH2 - the top upregulated gene along the trajectory - reverts tumor progression and macrophage polarization. Finally, a user-friendly web-resource is provided enabling the investigation of dynamic transcriptional perturbations linked to disease progression.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8640014 | PMC |
| http://dx.doi.org/10.1038/s41467-021-26840-5 | DOI Listing |
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