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Bottoni, Giulia; Katarkar, Atul; Tassone, Beatrice; Ghosh, Soumitra; Clocchiatti, Andrea; Goruppi, Sandro; Bordignon, Pino; Jafari, Paris; Tordini, Fabio; Lunardi, Thomas; Hoetzenecker, Wolfram; Neel, Victor; Lingner, Joachim; Paolo Dotto, G
Nature communications, 08/2019, Letnik: 10, Številka: 1Journal Article
Genomic instability is a hallmark of cancer. Whether it also occurs in Cancer Associated Fibroblasts (CAFs) remains to be carefully investigated. Loss of CSL/RBP-Jκ, the effector of canonical NOTCH signaling with intrinsic transcription repressive function, causes conversion of dermal fibroblasts into CAFs. Here, we find that CSL down-modulation triggers DNA damage, telomere loss and chromosome end fusions that also occur in skin Squamous Cell Carcinoma (SCC)-associated CAFs, in which CSL is decreased. Separately from its role in transcription, we show that CSL is part of a multiprotein telomere protective complex, binding directly and with high affinity to telomeric DNA as well as to UPF1 and Ku70/Ku80 proteins and being required for their telomere association. Taken together, the findings point to a central role of CSL in telomere homeostasis with important implications for genomic instability of cancer stromal cells and beyond.
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JCR | SNIP | JCR | SNIP | JCR | SNIP | JCR | SNIP |
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in: SICRIS
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