Erratum to: BRCA1-regulated RRM2 expression protects glioblastoma cells from endogenous replication stress and promotes tumorigenicity (Nature Communications, (2016), 7, 1, (13398), 10.1038/ncomms13398);BRCA1-regulated RRM2 expression protects glioblastoma cells from endogenous replication stress and promotes tumorigenicity

Nature Communications

Volumn 7, Issue , 2016, Pages

  Rasmussen, Rikke D ^a   Gajjar, Madhavsai K ^a   Tuckova, Lucie ^a   Jensen, Kamilla E ^b   Maya Mendoza, Apolinar ^a   Holst, Camilla B ^a   Møllgaard, Kjeld ^c   Rasmussen, Jane S ^d   Brennum, Jannick ^d   Bartek, Jiri ^a,d,e,g   Syrucek, Martin ^f   Sedlakova, Eva ^b   Andersen, Klaus K ^a   Frederiksen, Marie H ^a   Hamerlik, Petra ^a,d  

^a DANISH CANCER SOCIETY RESEARCH CENTER   (Denmark)

^b PALACKÝ UNIVERSITY   (Czech Republic)

^c UNIVERSITY OF COPENHAGEN   (Denmark)

^d Mental Health Center Glostrup   (Denmark)

^e KAROLINSKA UNIVERSITY HOSPITAL   (Sweden)

^f NA HOMOLCE HOSPITAL   (Czech Republic)

^g KAROLINSKA INSTITUTE   (Sweden)

Author keywords

[No Author keywords available]

Indexed keywords

3 AMINOPICOLINALDEHYDE THIOSEMICARBAZONE; BRCA1 PROTEIN; NICOTINAMIDE ADENINE DINUCLEOTIDE ADENOSINE DIPHOSPHATE RIBOSYLTRANSFERASE; RIBONUCLEOTIDE REDUCTASE; RIBONUCLEOTIDE REDUCTASE CATALYTIC SUBUNIT M2; UNCLASSIFIED DRUG; BRCA1 PROTEIN, HUMAN; RIBONUCLEOSIDE DIPHOSPHATE REDUCTASE; RIBONUCLEOTIDE REDUCTASE M2;

CANCER; CELLS AND CELL COMPONENTS; GENE EXPRESSION; GENETIC ANALYSIS; INHIBITOR; INSTABILITY; SURVIVAL; TUMOR;

ANIMAL CELL; ANIMAL EXPERIMENT; ANIMAL MODEL; ANIMAL TISSUE; APOPTOSIS; ARTICLE; ASTROCYTOMA; CANCER GROWTH; CANCER PATIENT; CANCER SURVIVAL; CARCINOGENESIS; CELL VIABILITY; CONTROLLED STUDY; DNA DAMAGE; DNA DAMAGE CHECKPOINT; FEMALE; GLIOBLASTOMA; GLIOBLASTOMA CELL LINE; HUMAN; HUMAN CELL; HUMAN TISSUE; MAJOR CLINICAL STUDY; MOUSE; NEUROPATHOLOGY; NEUROPROTECTION; NONHUMAN; PHENOTYPE; PROTEIN DEPLETION; PROTEIN EXPRESSION; PROTEIN FUNCTION; REGULATORY MECHANISM; RETROSPECTIVE STUDY; S PHASE CELL CYCLE CHECKPOINT; ANIMAL; BAGG ALBINO MOUSE; BRAIN TUMOR; DNA REPLICATION; GENE EXPRESSION REGULATION; GENETICS; METABOLISM; NUDE MOUSE; PATHOLOGY; RNA INTERFERENCE; SURVIVAL ANALYSIS; TUMOR CELL CULTURE; TUMOR CELL LINE; XENOGRAFT;

ANIMALS; BRAIN NEOPLASMS; BRCA1 PROTEIN; CARCINOGENESIS; CELL LINE, TUMOR; DNA REPLICATION; GENE EXPRESSION REGULATION, NEOPLASTIC; GLIOBLASTOMA; HUMANS; MICE, INBRED BALB C; MICE, NUDE; RETROSPECTIVE STUDIES; RIBONUCLEOSIDE DIPHOSPHATE REDUCTASE; RNA INTERFERENCE; SURVIVAL ANALYSIS; TRANSPLANTATION, HETEROLOGOUS; TUMOR CELLS, CULTURED;

EID: 84995428246     PISSN: None     EISSN: 20411723     Source Type: Journal    
DOI: 10.1038/s41467-018-07892-6     Document Type: Erratum

References (62)

1. Zhang, J. The role of BRCA1 in homologous recombination repair in response to replication stress: significance in tumorigenesis and cancer therapy. Cell Biosci. 3, 11 (2013).
2. Schlacher, K.,Wu, H. & Jasin, M. A distinct replication fork protection pathway connects Fanconi anemia tumor suppressors to RAD51-BRCA1/2. Cancer Cell 22, 106-116 (2012).
3. Ying, S., Hamdy, F. C. & Helleday, T. Mre11-dependent degradation of stalled DNA replication forks is prevented by BRCA2 and PARP1. Cancer Res. 72, 2814-2821 (2012).
4. Liu, S. et al. Distinct roles for DNA-PK, ATM and ATR in RPA phosphorylation and checkpoint activation in response to replication stress. Nucleic Acids Res. 40, 10780-10794 (2012).
5. Toledo, L. I. et al. ATR prohibits replication catastrophe by preventing global exhaustion of RPA. Cell 155, 1088-1103 (2013).
6. Krejci, L., Altmannova, V., Spirek, M. & Zhao, X. Homologous recombination and its regulation. Nucleic Acids Res. 40, 5795-5818 (2012).
7. Burrell, R. A. et al. Replication stress links structural and numerical cancer chromosomal instability. Nature 494, 492-496 (2013).
8. Da-Re, C. & Halazonetis, T. D. DNA replication stress as an Achilles' heel of cancer. Oncotarget 6, 1-2 (2015).
9. Lukas, C. et al. 53BP1 nuclear bodies form around DNA lesions generated by mitotic transmission of chromosomes under replication stress. Nat. Cell. Biol. 13, 243-253 (2011).
10. Pathania, S. et al. BRCA1 haploinsufficiency for replication stress suppression in primary cells. Nat. Commun. 5, 5496 (2014).
11. Pathania, S. et al. BRCA1 is required for postreplication repair after UVinduced DNA damage. Mol. Cell. 44, 235-251 (2011).
12. Bartkova, J. et al. DNA damage response as a candidate anti-cancer barrier in early human tumorigenesis. Nature 434, 864-870 (2005).
13. Bartkova, J. et al. Oncogene-induced senescence is part of the tumorigenesis barrier imposed by DNA damage checkpoints. Nature 444, 633-637 (2006).
14. Deng, C. X. & Wang, R. H. Roles of BRCA1 in DNA damage repair: a link between development and cancer. Hum. Mol. Genet. 12, R113-R123 (2003).
15. Xu, X. et al. Conditional mutation of Brca1 in mammary epithelial cells results in blunted ductal morphogenesis and tumour formation. Nat. Genet. 22, 37-43 (1999).
16. Navaraj, A. et al. Reduced cell death, invasive and angiogenic features conferred by BRCA1-deficiency in mammary epithelial cells transformed with H-Ras. Cancer Biol. Ther. 8, 2417-2444 (2009).
17. Zheng, L., Li, S., Boyer, T. G. & Lee, W. H. Lessons learned from BRCA1 and BRCA2. Oncogene 19, 6159-6175 (2000).
18. Helleday, T. The underlying mechanism for the PARP and BRCA synthetic lethality: clearing up the misunderstandings. Mol. Oncol. 5, 387-393 (2011).
19. Lord, C. J. & Ashworth, A. The DNA damage response and cancer therapy. Nature 481, 287-294 (2012).
20. Dedes, K. J. et al. Synthetic lethality of PARP inhibition in cancers lacking BRCA1 and BRCA2 mutations. Cell Cycle 10, 1192-1199 (2011).
21. Chalmers, A. J. Overcoming resistance of glioblastoma to conventional cytotoxic therapies by the addition of PARP inhibitors. Anticancer Agents Med. Chem. 10, 520-533 (2010).
22. Venere, M. et al. Therapeutic targeting of constitutive PARP activation compromises stem cell phenotype and survival of glioblastoma-initiating cells. Cell Death Differ. 21, 258-269 (2014).
23. Bartek, J., Mistrik, M. & Bartkova, J. Thresholds of replication stress signaling in cancer development and treatment. Nat. Struct. Mol. Biol. 19, 5-7 (2012).
24. Cloughesy, T. F., Cavenee, W. K. & Mischel, P. S. Glioblastoma: from molecular pathology to targeted treatment. Annu. Rev. Pathol. 9, 1-25 (2014).
25. Halazonetis, T. D., Gorgoulis, V. G. & Bartek, J. An oncogene-induced DNA damage model for cancer development. Science 319, 1352-1355 (2008).
26. Squatrito, M. et al. Loss of ATM/Chk2/p53 pathway components accelerates tumor development and contributes to radiation resistance in gliomas. Cancer Cell 18, 619-629 (2010).
27. Di Micco, R. et al. Oncogene-induced senescence is a DNA damage response triggered by DNA hyper-replication. Nature 444, 638-642 (2006).
28. Gorgoulis, V. G. et al. Activation of the DNA damage checkpoint and genomic instability in human precancerous lesions. Nature 434, 907-913 (2005).
29. Lai, I. L. et al. Targeting the Warburg effect with a novel glucose transporter inhibitor to overcome gemcitabine resistance in pancreatic cancer cells. Carcinogenesis 35, 2203-2213 (2014).
30. Aird, K. M. et al. Suppression of nucleotide metabolism underlies the establishment and maintenance of oncogene-induced senescence. Cell Rep. 3, 1252-1265 (2013).
31. Nordlund, P. & Reichard, P. Ribonucleotide reductases. Annu. Rev. Biochem. 75, 681-706 (2006).
32. Gorski, J. J. et al. Profiling of the BRCA1 transcriptome through microarray and ChIP-chip analysis. Nucleic Acids Res. 39, 9536-9548 (2011).
33. Zhou, B. & Yen, Y. Characterization of the human ribonucleotide reductase M2 subunit gene; genomic structure and promoter analyses. Cytogenet. Cell Genet. 95, 52-59 (2001).
34. Wang, N. et al. Increased expression of RRM2 by human papillomavirus E7 oncoprotein promotes angiogenesis in cervical cancer. Br. J. Cancer 110, 1034-1044 (2014).
35. Kunos, C. A. et al. Radiochemotherapy plus 3-aminopyridine-2-carboxaldehyde thiosemicarbazone (3-AP, NSC #663249) in advanced-stage cervical and vaginal cancers. Gynecol. Oncol. 130, 75-80 (2013).
36. Jiang, Z. G., Lebowitz, M. S. & Ghanbari, H. A. Neuroprotective activity of 3-aminopyridine-2-carboxaldehyde thiosemicarbazone (PAN-811), a cancer therapeutic agent. CNS Drug Rev. 12, 77-90 (2006).
37. Lane, D. J. et al. Expanding horizons in iron chelation and the treatment of cancer: role of iron in the regulation of ER stress and the epithelialmesenchymal transition. Biochim. Biophys. Acta 1845, 166-181 (2014).
38. Rasmussen, R. D., Gajjar, M. K., Jensen, K. E. & Hamerlik, P. Enhanced efficacy of combined HDAC and PARP targeting in glioblastoma. Mol. Oncol. 10, 751-763 (2016).
39. Verhaak, R. G. et al. Integrated genomic analysis identifies clinically relevant subtypes of glioblastoma characterized by abnormalities in PDGFRA, IDH1, EGFR, and NF1. Cancer Cell 17, 98-110 (2010).
40. Macheret, M. & Halazonetis, T. D. DNA replication stress as a hallmark of cancer. Annu. Rev. Pathol. 10, 425-448 (2015).
41. Li, L. BRCA1 forks over new roles in DNA-damage response-before and beyond the breaks. Mol. Cell 44, 174-176 (2011).
42. James, C. R., Quinn, J. E., Mullan, P. B., Johnston, P. G. & Harkin, D. P. BRCA1, a potential predictive biomarker in the treatment of breast cancer. Oncologist 12, 142-150 (2007).
43. De Luca, P. et al. BRCA1 loss induces GADD153-mediated doxorubicin resistance in prostate cancer. Mol. Cancer Res. 9, 1078-1090 (2011).
44. Deng, C. X. BRCA1: cell cycle checkpoint, genetic instability, DNA damage response and cancer evolution. Nucleic Acids Res. 34, 1416-1426 (2006).
45. Thompson, M. E., Jensen, R. A., Obermiller, P. S., Page, D. L. & Holt, J. T. Decreased expression of BRCA1 accelerates growth and is often present during sporadic breast cancer progression. Nat. Genet. 9, 444-450 (1995).
46. Tominaga, Y. et al. Genistein inhibits Brca1 mutant tumor growth through activation of DNA damage checkpoints, cell cycle arrest, and mitotic catastrophe. Cell Death Differ. 14, 472-479 (2007).
47. Yuli, C. et al. BRCA1a has antitumor activity in TN breast, ovarian and prostate cancers. Oncogene 26, 6031-6037 (2007).
48. Holt, J. T. et al. Growth retardation and tumour inhibition by BRCA1. Nat. Genet. 12, 298-302 (1996).
49. Pfister, S. X. et al. Inhibiting WEE1 selectively kills histone H3K36me3-deficient cancers by dNTP starvation. Cancer Cell 28, 557-568 (2015).
50. Poli, J. et al. dNTP pools determine fork progression and origin usage under replication stress. EMBO J. 31, 883-894 (2012).
51. Chabes, A. & Thelander, L. Controlled protein degradation regulates ribonucleotide reductase activity in proliferating mammalian cells during the normal cell cycle and in response to DNA damage and replication blocks. J. Biol. Chem. 275, 17747-17753 (2000).
52. Pulvers, J. N. & Huttner, W. B. Brca1 is required for embryonic development of the mouse cerebral cortex to normal size by preventing apoptosis of early neural progenitors. Development 136, 1859-1868 (2009).
53. MacLachlan, T. K., Takimoto, R. & El-Deiry, W. S. BRCA1 directs a selective p53-dependent transcriptional response towards growth arrest and DNA repair targets. Mol. Cell Biol. 22, 4280-4292 (2002).
54. D'Angiolella, V. et al. Cyclin F-mediated degradation of ribonucleotide reductase M2 controls genome integrity and DNA repair. Cell 149, 1023-1034 (2012).
55. Xu, X. et al. Broad overexpression of ribonucleotide reductase genes in mice specifically induces lung neoplasms. Cancer. Res. 68, 2652-2660 (2008).
56. Bartkova, J. et al. Replication stress and oxidative damage contribute to aberrant constitutive activation of DNA damage signalling in human gliomas. Oncogene 29, 5095-5102 (2010).
57. Jones, R. M. & Petermann, E. Replication fork dynamics and the DNA damage response. Biochem. J. 443, 13-26 (2012).
58. Luo, J., Solimini, N. L. & Elledge, S. J. Principles of cancer therapy: oncogene and non-oncogene addiction. Cell 136, 823-837 (2009).
59. Louis, D. N. et al. The 2007 WHO classification of tumours of the central nervous system. Acta Neuropathol. 114, 97-109 (2007).
60. Hamerlik, P. et al. Autocrine VEGF-VEGFR2-Neuropilin-1 signaling promotes glioma stem-like cell viability and tumor growth. J. Exp. Med. 209, 507-520 (2012).
61. Jackson, D. A. & Pombo, A. Replicon clusters are stable units of chromosome structure: evidence that nuclear organization contributes to the efficient activation and propagation of S phase in human cells. J. Cell Biol. 140, 1285-1295 (1998).
62. Singh, N. P., McCoy, M. T., Tice, R. R. & Schneider, E. L. A simple technique for quantitation of low levels of DNA damage in individual cells. Exp. Cell Res. 175, 184-191 (1988).