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| Format: | Recurso digital |
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Zenodo
2025
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| Online Access: | https://doi.org/10.5281/zenodo.14602347 |
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Table of Contents:
- <p>We discovered aberrant activation of Xist in cancer, the non-coding RNA that silences duplicate X chromosomes in females to execute dosage compensation, by studying whole transcription in p53-sufficient and p53-deficient cancer cells (1). We next described high levels of Xist expression that could be triggered by mutation or loss of either of two major tumor suppressors, p53 or Rb (1, 2). We demonstrated a function for Xist in activation and repression of solid tumor gene expression, in humans with breast cancer, driven by p53 loss, and demonstrated a role for the expression of these Xist-modulated genes in subtype selection (instruction of tumor lineage) in breast cancer (3, 4). We also described the existence of Xist ribonucleic protein (Xist RNP) complexes that putatively functioned to dynamically control gene expression in transformed cells (5). </p> <p>We describe here Xist control of transcriptional targets in the lung during transformation (6-9). We demonstrate control of MYC gene expression by Xist and a role for this gene expression control in subtype selection in non-small cell lung cancer. Xist activation is likely a widespread and relatively common biological phenomena during solid tumor development and disease progression driven by loss of tumor suppressor (p53/Rb) function. Xist influences subtype selection in non-small cell lung cancer by modulating expression of a wide range of transcriptional targets.</p> <p> </p>