APOBEC3B gene overexpression in non-small-cell lung cancer

被引:25
作者
Sasaki, Hidefumi [1 ]
Suzuki, Ayumi [1 ]
Tatematsu, Tsutomu [1 ]
Shitara, Masayuki [1 ]
Hikosaka [1 ]
Okuda, Katsuhiro [1 ]
Moriyama, Satoru [1 ]
Yano, Motoki [1 ]
Fujii, Yoshitaka [1 ]
机构
[1] Nagoya City Univ, Grad Sch Med Sci, Dept Oncol Immunol & Surg, Nagoya, Aichi 4678601, Japan
基金
日本学术振兴会;
关键词
APOBEC3B; mutation; lung cancer; epidermal growth factor receptor; LightCycler;
D O I
10.3892/br.2014.256
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
Recent study results have demonstrated that a subclass of apolipoprotein B mRNA-editing enzyme, catalytic polypeptide-like (APOBEC) cytidine deaminase may induce mutation clusters in various types of cancer. From the Cancer Genome Altas, an APOBEC mutation pattern was identified in bladder, cervical, breast, head and neck and lung cancers. In the present study, APOBEC3B mRNA expression was investigated using quantitative reverse transcription-polymerase chain reaction (RT-qPCR) assay using LightCycler in surgically treated non-small-cell lung cancer (NSCLC) cases. Additionally, 88 surgically removed Japanese NSCLC cases were analyzed for mRNA level. The results showed that APOBEC3B/beta-actin mRNA levels were significantly higher in lung cancer (1,598.481 +/- 6,465.781) when compared to adjacent normal lung tissues (2,116.639 +/- 8,337.331, P=0.5453). The tumor/normal (T/N) ratio of APOBEC3B/beta-actin mRNA levels was not different within the gender, age, smoking status and pathological stages. The T/N ratio of APOBEC3B/beta-actin mRNA levels was not significantly different in epidermal growth factor receptor (EGFR) or Kras mutation-positive cases as compared to the wild-type cases.
引用
收藏
页码:392 / 395
页数:4
相关论文
共 21 条
  • [1] Comparison of the differential context-dependence of DNA deamination by APOBEC enzymes:: Correlation with mutation spectra in vivo
    Beale, RCL
    Petersen-Mahrt, SK
    Watt, IN
    Harris, RS
    Rada, C
    Neuberger, MS
    [J]. JOURNAL OF MOLECULAR BIOLOGY, 2004, 337 (03) : 585 - 596
  • [2] APOBEC3B is an enzymatic source of mutation in breast cancer
    Burns, Michael B.
    Lackey, Lela
    Carpenter, Michael A.
    Rathore, Anurag
    Land, Allison M.
    Leonard, Brandon
    Refsland, Eric W.
    Kotandeniya, Delshanee
    Tretyakova, Natalia
    Nikas, Jason B.
    Yee, Douglas
    Temiz, Nuri I. A.
    Donohue, Duncan E.
    McDougle, Rebecca M.
    Brown, William L.
    Law, Emily K.
    Harris, Reuben S.
    [J]. NATURE, 2013, 494 (7437) : 366 - 370
  • [3] Base Damage within Single-Strand DNA Underlies In Vivo Hypermutability Induced by a Ubiquitous Environmental Agent
    Chan, Kin
    Sterling, Joan F.
    Roberts, Steven A.
    Bhagwat, Ashok S.
    Resnick, Michael A.
    Gordenin, Dmitry A.
    [J]. PLOS GENETICS, 2012, 8 (12):
  • [4] Conticello Silvestro G, 2007, Adv Immunol, V94, P37, DOI 10.1016/S0065-2776(06)94002-4
  • [5] Creative deaminases, self-inflicted damage, and genome evolution
    Conticello, Silvestro G.
    [J]. EFFECTS OF GENOME STRUCTURE AND SEQUENCE ON VARIATION AND EVOLUTION, 2012, 1267 : 79 - 85
  • [6] Ginsberg RJ, 1993, PRINCIPLES PRACTICE, P673
  • [7] Hallmarks of Cancer: The Next Generation
    Hanahan, Douglas
    Weinberg, Robert A.
    [J]. CELL, 2011, 144 (05) : 646 - 674
  • [8] RNA editing enzyme APOBEC1 and some of its homologs can act as DNA mutators
    Harris, RS
    Petersen-Mahrt, SK
    Neuberger, MS
    [J]. MOLECULAR CELL, 2002, 10 (05) : 1247 - 1253
  • [9] AID/APOBEC cytosine deaminase induces genome-wide kataegis
    Lada, Artem G.
    Dhar, Alok
    Boissy, Robert J.
    Hirano, Masayuki
    Rubel, Aleksandr A.
    Rogozin, Igor B.
    Pavlov, Youri I.
    [J]. BIOLOGY DIRECT, 2012, 7
  • [10] APOBEC3A can activate the DNA damage response and cause cell-cycle arrest
    Landry, Sebastien
    Narvaiza, Inigo
    Linfesty, Daniel C.
    Weitzman, Matthew D.
    [J]. EMBO REPORTS, 2011, 12 (05) : 444 - 450