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DNA-dependent protein synthesis exhibited by cancer shed particulates

View ORCID ProfileVijay K. Ulaganathan, Axel Ullrich
doi: https://doi.org/10.1101/121186
Vijay K. Ulaganathan
Max Planck Institute of Biochemistry, Department of Molecular Biology, Am Klopferspitz, Martinsried 82152, Germany
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  • For correspondence: ulaganat@biochem.mpg.de ulaganat@icloud.com
Axel Ullrich
Max Planck Institute of Biochemistry, Department of Molecular Biology, Am Klopferspitz, Martinsried 82152, Germany
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Abstract

Genetic heterogeneity in tumours is the bonafide hallmark applicable to all cancer types (Burrell et al, 2013). Furthermore, deregulated ribosome biogenesis and elevated protein biosynthesis have been consistently associated with multiple cancer types (Ruggero, 2012; Ruggero & Pandolfi, 2003). We observed that under cultivation conditions almost all cancer cell types actively shed significant amount of particulates as compared to non-malignant cell lines requiring frequent changing of cultivation media. We therefore asked if cancer cell shed particulates might still retain biological activity associated with protein biosynthesis. Here, we communicate our observations of DNA-dependent protein biosynthetic activity exhibited by the cell-free particulates shed by the cancer cell lines. Using pulsed isotope labelling approach we confirmed the cell-free protein translation activity exhibited by particulates shed by various cancer cell lines. Interestingly, the bioactivity was largely dependent on temperature, pH and on 3’-DNA elements. Our results demonstrate that cancer shed particulates are biologically active and may potentially drive expression of tissue non-specific promoters in distant organs.

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Posted March 27, 2017.
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DNA-dependent protein synthesis exhibited by cancer shed particulates
Vijay K. Ulaganathan, Axel Ullrich
bioRxiv 121186; doi: https://doi.org/10.1101/121186
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DNA-dependent protein synthesis exhibited by cancer shed particulates
Vijay K. Ulaganathan, Axel Ullrich
bioRxiv 121186; doi: https://doi.org/10.1101/121186

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