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DNA Repair: a Single-Edged Sword?

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DNA Repair: a Single-Edged Sword? RESEARCH HIGHLIGHTS DNA REPAIR Therefore, the mutagenic effect of TLS could be a crucial determinant of therapeutic response. However, A single-edged sword? other studies have shown that, in cells that can tolerate the loss of TLS, Deficiencies in DNA repair processes persistence of unrepaired DNA dam- Rev3l deletion causes the collapse of modulate both tumorigenesis and age. shRNA-transduced NSCLC cells replication forks, leading to chromo- chemotherapy response. Therapeutic injected into the tail vein colonized somal instability and thus promoting inhibition of DNA repair can sen- the lung and allowed assessment mutagenesis. sitize cancer cells to chemotherapy of the in vivo therapeutic response — It will be interesting to see whether or can function as a synthetic lethal REV3L knockdown slowed NSCLC the effects of cancer cell-specific TLS strategy for the treatment of cancers tumour progression and prolonged gene knockdown can be replicated with certain DNA repair defects. the survival of the mice. using systemic delivery of TLS- However, DNA repair inhibition is To investigate the mutagenic role targeted therapeutics. The potential typically accompanied by the threat of TLS following chemotherapy treat- toxicity of a TLS-targeted agent of accelerated mutagenesis. Two ment, both groups used a cellular towards normal cells would need to recent papers suggest that targeting mutagenesis assay, in which muta- be considered and carefully balanced, DNA repair mechanisms is not tions at the mouse hypoxanthine as knock out of Rev3l in mice is always a double-edged sword: repres- guanine phosphoribosyl transferase embryonic lethal, in contrast to the sion of translesion synthesis (TLS) (Hprt) locus, acquired during chemo- absence of obvious viability defects can not only sensitize chemoresistant therapy treatment, result in resistance in REV3L-knockdown cells. Finally, tumours to therapy but can also keep to 6-thioguanine (6-TG). A reduction it remains to be seen whether TLS mutagenesis in check. in mutagenesis on TLS suppression inhibition can be selectively lethal to TLS is a DNA damage tolerance was evident in REV3L-downregulated cancer cells with particular types of mechanism whereby alternative DNA NSCLC cells treated with cisplatin. DNA repair deficiencies. polymerases use error-prone REV1-downregulated lymphomas Darren J. Burgess DNA synthesis to bypass bulky DNA were not immediately sensitized to an ORIGINAL RESEARCH PAPERS Xie, K., et al. lesions, such as those caused by alkylating agent, cyclophosphamide, Error-prone translesion synthesis mediates chemotherapeutics. Components either in vitro or in vivo. However, acquired chemoresistance. Proc. Natl Acad. Sci. USA 107, 20792–20797 (2010) | Doles, J., et al. of TLS include REV3L (a subunit of following successive rounds of treat- Suppression of Rev3, the catalytic subunit of DNA polymerase-ζ) and REV1 ment, REV1 knockdown delayed the Polζ, sensitizes drug-resistant lung tumors to (a TLS scaffold protein). To inves- emergence of therapeutic resistance, chemotherapy. Proc. Natl Acad. Sci. USA 107, 20786–20791 (2010) tigate the role of TLS in therapy possibly owing to fewer mutations. response and mutagenesis, both groups combined tractable mouse models of cancer with short hairpin RNA (shRNA)-mediated depletion of TLS components. Graham Walker and colleagues used a chemosensitive Eμ-Myc lymphoma model and showed that knock down of REV3L or REV1 further sensitized lymphomas to the crosslinking agent cisplatin. To inves- tigate whether TLS repression could also increase the therapeutic response of chemorefractory tumours, Mike Hemann and colleagues knocked down REV3L in a KrasG12D;Trp53–/– mouse model of non-small-cell lung cancer (NSCLC). REV3L knockdown markedly sensitized NSCLC cells to cisplatin in vitro, accompanied by a Smith Neil NATURE REVIEWS | CANCER VOLUME 11 | JANUARY 2011 © 2011 Macmillan Publishers Limited. All rights reserved.
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