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PLOS ONE  2013 

There Is No Association between MicroRNA Gene Polymorphisms and Risk of Triple Negative Breast Cancer in a Chinese Han Population

DOI: 10.1371/journal.pone.0060195

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Abstract:

Triple-negative breast cancer (TNBC) is defined by the lack of the expression of estrogen receptor (ER), progesterone receptor (PR) and human epidermal growth factor receptor 2 (HER2). It is characterized by aggressive behavior, poor prognosis and lack of targeted therapies. MicroRNA (miRNA) as a novel modulator of gene expression has played an important regulatory role in the malignancy. Dysregulation and/or mutation of the miRNAs may also contribute to the TNBC susceptibility since it is associated with the expression of ER, PR and HER2. Single nucleotide polymorphisms (SNPs) in miRNAs may be extremely relevant for TNBC. We tried to validate the hypothesis that genetic variations in miRNA are associated with TNBC development, and identify candidate biomarkers for TNBC susceptibility and clinical treatment. We screened the genetic variants in all miRNA genes listed in the public database miRBase and NCBI. A total of 23 common SNPs in 22 miRNAs, which tagged the known common variants in the Chinese Han people with a minor allele frequency greater than 0.05, were genotyped. This case-control study involved 191 patients with TNBC and 192 healthy female controls. Frequencies of SNPs were compared between cases and controls to identify the SNPs associated with TNBC susceptibility. No significant association was found between TNBC risk and the SNPs in the miRNA genes in the Chinese Han people (P>0.05), but this warrants further studies.

References

[1]  Bauer KR, Brown M, Cress RD, Parise CA, Caggiano V (2007) Descriptive analysis of estrogen receptor (ER)-negative, progesterone receptor (PR)-negative, and HER2-negative invasive breast cancer, the so-called triple-negative phenotype: a population-based study from the California cancer Registry. Cancer 109(9): 1721–1728.
[2]  Irvin WJ Jr, Carey LA (2008) What is triple-negative breast cancer? Eur J Cancer 44(18): 2799–2805.
[3]  Pal SK, Childs BH, Pegram M (2011) Triple negative breast cancer: unmet medical needs. Breast Cancer Res Treat 125(3): 627–636.
[4]  Foulkes WD, Smith IE, Reis-Filho JS (2010) Triple-negative breast cancer. N Engl J Med 363(20): 1938–1948.
[5]  Amirikia KC, Mills P, Bush J, Newman LA (2011) Higher population-based incidence rates of triple-negative breast cancer among young African-American women: Implications for breast cancer screening recommendations. Cancer 117(12): 2747–2753.
[6]  Cleator S, Heller W, Coombes RC (2007) Triple-negative breast cancer: therapeutic options. Lancet Oncol 8(3): 235–244.
[7]  Perez EA, Moreno-Aspitia A, Aubrey Thompson E, Andorfer CA (2010) Adjuvant therapy of triple negative breast cancer. Breast Cancer Res Treat 120(2): 285–291.
[8]  Ma K, Chau WW, Wong CH, Wong K, Fung N, et al. (2012) Triple Negative Status is a Poor Prognostic Indicator in Chinese Women with Breast Cancer: a Ten Year Review. Asian Pac J Cancer Prev 13(5): 2109–2114.
[9]  Morris GJ, Naidu S, Topham AK, Guiles F, Xu Y, et al. (2007) Differences in breast carcinoma characteristics in newly diagnosed African-American and Caucasian patients: a single-institution compilation compared with the National Cancer Institute’s Surveillance, Epidemiology, and End Results database. Cancer 110(4): 876–884.
[10]  Zeng Y, Wagner EJ, Cullen BR (2002) Both natural and designed micro RNAs can inhibit the expression of cognate mRNAs when expressed in human cells. Mol Cell 9(6): 1327–1333.
[11]  Calin GA, Sevignani C, Dumitru CD, Hyslop T, Noch E, et al. (2004) Human microRNA genes are frequently located at fragile sites and genomic regions involved in cancers. Proc Natl Acad Sci U S A 101(9): 2999–3004.
[12]  Farazi TA, Spitzer JI, Morozov P, Tuschl T (2011) miRNAs in human cancer. J Pathol 223(2): 102–115.
[13]  He L, He X, Lim LP, de Stanchina E, Xuan Z, et al. (2007) A microRNA component of the p53 tumour suppressor network. Nature 447(7148): 1130–1134.
[14]  Iorio MV, Ferracin M, Liu CG, Veronese A, Spizzo R, et al. (2005) MicroRNA gene expression deregulation in human breast cancer. Cancer Res 65(16): 7065–7070.
[15]  Adams BD, Furneaux H, White BA (2007) The micro-ribonucleic acid (miRNA) miR-206 targets the human estrogen receptor-alpha (ERalpha) and represses ERalpha messenger RNA and protein expression in breast cancer cell lines. Mol Endocrinol 21(5): 1132–1147.
[16]  Matthew A Saunders, Han Liang, Wen-Hsiung Li (2007) Human polymorphism at microRNAs and microRNA target sites. Proc Natl Acad Sci U S A 104(9): 3300–3305.
[17]  Duan R, Pak CH, Jin P (2007) Single nucleotide polymorphism associated with mature miR-125a alters the processing of pri-miRNA. Hum Mol Genet 16 (9): 1124–1131.
[18]  Nicoloso MS, Sun H, Spizzo R, Kim H, Wickramasinghe P, et al. (2010) Single-nucleotide polymorphisms inside microRNA target sites influence tumor susceptibility. Cancer Res 70(7): 2789–2798.
[19]  Ye Y, Wang KK, Gu J, Yang H, Lin J, et al. (2008) Genetic variations in microRNA-related genes are novel susceptibility loci for esophageal cancer risk. Cancer Prev Res (Phila) 1(6): 460–469.
[20]  Chin LJ, Ratner E, Leng S, Zhai R, Nallur S, et al. (2008) A SNP in a let-7 microRNA complementary site in the KRAS 3′ untranslated region increases non-small cell lung cancer risk. Cancer Res 68(20): 8535–8540.
[21]  Horikawa Y, Wood CG, Yang H, Zhao H, Ye Y, et al. (2008) Single nucleotide polymorphisms of microRNA machinery genes modify the risk of renal cell carcinoma. Clin Cancer Res 14(23): 7956–7962.
[22]  Yang H, Dinney CP, Ye Y, Zhu Y, Grossman HB, et al. (2008) Evaluation of genetic variants in microRNA-related genes and risk of bladder cancer. Cancer Res 68(7): 2530–2537.
[23]  Hu Z, Liang J, Wang Z, Tian T, Zhou X, et al. (2009) Common genetic variants in pre-microRNAs were associated with increased risk of breast cancer in Chinese women. Hum Mutat 30(1): 79–84.
[24]  Yang R, Schlehe B, Hemminki K, Sutter C, Bugert P, et al. (2010) A genetic variant in the pre-miR-27a oncogene is associated with a reduced familial breast cancer risk. Breast Cancer Res Treat 121(3): 693–702.
[25]  Shi YY, He L (2005) SHEsis, a powerful software platform for analyses of linkage disequilibrium, haplotype construction, and genetic association at polymorphism loci. Cell Res 15(2): 97–98.
[26]  Diederichs S, Haber DA (2005) Sequence variations of microRNAs in human cancer: alterations in predicted secondary structure do not affect processing. Cancer Res 66(12): 6097–6104.
[27]  Iwai N, Naraba H (2005) Polymorphisms in human pre-miRNAs. Biochem Biophys Res Commun 331(4): 1439–1444.
[28]  Nicoloso MS, Sun H, Spizzo R, Kim H, Wickramasinghe P (2010) et?al (2010) Single-nucleotide polymorphisms inside microRNA target sites influence tumor susceptibility. Cancer Res 70(7): 2789–2798.
[29]  Liang D, Meyer L, Chang DW, Lin J, Pu X, et al. (2010) Genetic variants in MicroRNA biosynthesis pathways and binding sites modify ovarian cancer risk, survival, and treatment response. Cancer Res 70(23): 9765–9776.
[30]  Hayashita Y, Osada H, Tatematsu Y, Yamada H, Yanagisawa K, et al. (2005) A polycistronic microRNA cluster, miR-17–92, is overexpressed in human lung cancers and enhances cell proliferation. Cancer Res 65(21): 9628–9632.
[31]  Ota A, Tagawa H, Karnan S, Tsuzuki S, Karpas A, et al. (2004) Identification and characterization of a novel gene, C13orf25, as a target for 13q31-q32 amplification in malignant lymphoma. Cancer Res 64(9): 3087–3095.
[32]  Rinaldi A, Poretti G, Kwee I, Zucca E, Catapano CV, et al. (2007) Concomitant MYC and microRNA cluster miR-17–92 (C13orf25) amplification in human mantle cell lymphoma. Leuk Lymphoma 48(2): 410–412.
[33]  Tagawa H, Karube K, Tsuzuki S, Ohshima K, Seto M (2007) Synergistic action of the microRNA-17 polycistron and Myc in aggressive cancer development. Cancer Sci 98(9): 1482–1490.
[34]  Calin GA, Dumitru CD, Shimizu M, Bichi R, Zupo S, et al. (2002) Frequent deletions and down-regulation of micro- RNA genes miR15 and miR16 at 13q14 in chronic lymphocytic leukemia. Proc Natl Acad Sci U S A 99(24): 15524–15529.
[35]  Chang TC, Wentzel EA, Kent OA, Ramachandran K, Mullendore M, et al. (2007) Transactivation of miR-34a by p53 broadly influences gene expression and promotes apoptosis. Mol Cell 26(5): 745–752.
[36]  Raver-Shapira N, Marciano E, Meiri E, Spector Y, Rosenfeld N, et al. (2007) Transcriptional activation of miR-34a contributes to p53-mediated apoptosis. Mol Cell 26(5): 731–743.
[37]  Tarasov V, Jung P, Verdoodt B, Lodygin D, Epanchintsev A, et al. (2007) Differential regulation of microRNAs by p53 revealed by massively parallel sequencing: miR-34a is a p53 target that induces apoptosis and G1-arrest. Cell Cycle 6(13): 1586–1593.
[38]  Wang TY, Dong YY, Li HY, Li X (2010) Molecular evolution and regulatory mechanism of microRNAs. HEREDITAS 32(9): 874–880.

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