Nukleosidoen bidezko tratamenduak ondesteko minbizi zelulen egonkortasun genomikoa berreskuratzen du baina ez du migratzeko gaitasuna ekiditen
DOI:
https://doi.org/10.26876/ikergazte.vi.04.18Keywords:
E2F1/2, colorectal cancer, genome instability, migration, nucleosidesAbstract
Genome instability is a hallmark of cancer. In fact, the loss of genome integrity grants cancer cells with several advantages that facilitate tumor progression and the ability to develop metastasis. In this work, we show that in colorectal cancer cells the absence of E2F1 and E2F2 transcription factors induces genomic instability. Importantly, the loss of E2F1/2 activity increases cell migration capacity and prometastatic traits. To test whether these two phenotypes were related in our model, we exogenously supplied cells with nucleosides to rescue genomic instability. However, increased migration capacity induced by E2F1/2 loss was not affected by nucleoside treatment. Therefore, the loss of E2F activity promotes genome instability and migration capacity through independent mechanisms.
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