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Vol 88, No 10 (2017)
Research paper
Published online: 2017-10-31
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Dysregulation of microRNAs in triple-negative breast cancer

Sylwia Paszek12, Natalia Gabło12, Edyta Barnaś3, Małgorzata Szybka4, Jan Morawiec5, Agnieszka Kołacińska56, Izabela Zawlik12
DOI: 10.5603/GP.a2017.0097
·
Pubmed: 29192413
·
Ginekol Pol 2017;88(10):530-536.
Affiliations
  1. Centre for Innovative Research in Medical and Natural Sciences, Faculty of Medicine, University of Rzeszow, Warzywna 1a, 35-959 Rzeszow, Poland
  2. Department of Genetics, Faculty of Medicine, University of Rzeszow, Kopisto 2a, 35-959 Rzeszow, Poland
  3. Institute of Obstetrics and Emergency Medicine, Faculty of Medicine, University of Rzeszow Poland, Pigonia 6, 35-959 Rzeszow, Poland
  4. Department of Microbiology and Laboratory Medical Immunology, Faculty of Medicine, Medical University of Lodz, Pomorska 251, 92-213 Lodz, Poland
  5. Department of Head and Neck Cancer Surgery, Medical University of Lodz, Paderewskiego 4, 93-509 Lodz, Poland
  6. Department of Surgical Oncology, Cancer Center, Copernicus Memorial Hospital,, Paderewskiego 4, 93-509 Lodz, Poland

open access

Vol 88, No 10 (2017)
ORIGINAL PAPERS Gynecology
Published online: 2017-10-31

Abstract

Objectives: Triple-negative breast cancer (TNBC) is an aggressive subtype of breast cancer with limited treatment options and poor prognosis. TNBC is usually diagnosed at a relatively young age and is characterized by high risk of developing metastases. Some epigenetic regulation of gene expression is associated with TNBC. Expression of microRNAs (miRNAs) can serve as a potential tool for identifying critical biomarkers in TNBC. The aim of our study is to examine expression of selected miRNAs in TNBC and to assess the relationship between miRNA expression and clinicopathological factors.

Material and methods: Expression levels of 19 selected miRNAs were compared between cancerous and normal breast tissues by use of qPCR method. We have evaluated the relationship between the expression level of miRNAs and clinicopathological factors such as: age, tumor size and lymph node status.

Results: We found that in TNBC tissues, when compared with normal breast tissues, the expression of miR-190a, miR- 136-5p and miR-126-5p was significantly reduced (p = 0.0041, p = 0.0007, p = 0.0007, respectively) whereas expression of miR-135b-5p and miR-182-5p was significantly increased (p = 0.0194, p = 0.0041, respectively). We found a linear trend for tumor size and expression of miR-126-5p (p = 0.0296) and miR-135b-5p (p = 0.0241).

Conclusions: Our study confirms that miRNA expression profile is dysregulated in TNBC patients compared to healthy controls. MiR-190a, miR-136-5p, miR-126-5p, miR-135b-5p and miR-182-5p may be associated with development and progression of TNBC

Abstract

Objectives: Triple-negative breast cancer (TNBC) is an aggressive subtype of breast cancer with limited treatment options and poor prognosis. TNBC is usually diagnosed at a relatively young age and is characterized by high risk of developing metastases. Some epigenetic regulation of gene expression is associated with TNBC. Expression of microRNAs (miRNAs) can serve as a potential tool for identifying critical biomarkers in TNBC. The aim of our study is to examine expression of selected miRNAs in TNBC and to assess the relationship between miRNA expression and clinicopathological factors.

Material and methods: Expression levels of 19 selected miRNAs were compared between cancerous and normal breast tissues by use of qPCR method. We have evaluated the relationship between the expression level of miRNAs and clinicopathological factors such as: age, tumor size and lymph node status.

Results: We found that in TNBC tissues, when compared with normal breast tissues, the expression of miR-190a, miR- 136-5p and miR-126-5p was significantly reduced (p = 0.0041, p = 0.0007, p = 0.0007, respectively) whereas expression of miR-135b-5p and miR-182-5p was significantly increased (p = 0.0194, p = 0.0041, respectively). We found a linear trend for tumor size and expression of miR-126-5p (p = 0.0296) and miR-135b-5p (p = 0.0241).

Conclusions: Our study confirms that miRNA expression profile is dysregulated in TNBC patients compared to healthy controls. MiR-190a, miR-136-5p, miR-126-5p, miR-135b-5p and miR-182-5p may be associated with development and progression of TNBC

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Keywords

TNBC, microRNA expression, biomarkers

About this article
Title

Dysregulation of microRNAs in triple-negative breast cancer

Journal

Ginekologia Polska

Issue

Vol 88, No 10 (2017)

Article type

Research paper

Pages

530-536

Published online

2017-10-31

Page views

2907

Article views/downloads

2253

DOI

10.5603/GP.a2017.0097

Pubmed

29192413

Bibliographic record

Ginekol Pol 2017;88(10):530-536.

Keywords

TNBC
microRNA expression
biomarkers

Authors

Sylwia Paszek
Natalia Gabło
Edyta Barnaś
Małgorzata Szybka
Jan Morawiec
Agnieszka Kołacińska
Izabela Zawlik

References (35)
  1. Siegel R, Ma J, Zou Z, et al. Cancer statistics, 2014. CA Cancer J Clin. 2014; 64(1): 9–29.
    CrossRefPubMed
  2. Cheang MCU, Voduc D, Bajdik C, et al. Basal-like breast cancer defined by five biomarkers has superior prognostic value than triple-negative phenotype. Clin Cancer Res. 2008; 14(5): 1368–1376.
    CrossRefPubMed
  3. Hudis CA, Gianni L. Triple-negative breast cancer: an unmet medical need. Oncologist. 2011; 16 Suppl 1: 1–11.
    CrossRefPubMed
  4. Godfrey SS, Moses MM, Rorie CJ. Cancer Associated MicroRNAs are Differentially Expressed in Triple Negative Breast Cancer and Normal Breast Cells. Int J Surg Res. 2015: 4–78.
  5. Boyle P. Triple-negative breast cancer: epidemiological considerations and recommendations. Ann Oncol. 2012; 23 Suppl 6: vi7–v12.
    CrossRefPubMed
  6. Anders C, Carey LA. Understanding and treating triple-negative breast cancer. Oncology (Williston Park). 2008; 22(11): 1233–9; discussion 1239.
    PubMed
  7. O'Reilly EA, Gubbins L, Sharma S, et al. The fate of chemoresistance in triple negative breast cancer (TNBC). BBA Clin. 2015; 3: 257–275.
    CrossRefPubMed
  8. D'Ippolito E, Iorio MV. MicroRNAs and triple negative breast cancer. Int J Mol Sci. 2013; 14(11): 22202–22220.
    CrossRefPubMed
  9. Pillai RS. MicroRNA function: multiple mechanisms for a tiny RNA? RNA. 2005; 11(12): 1753–1761.
    CrossRefPubMed
  10. Dvinge H, Git A, Gräf S, et al. The shaping and functional consequences of the microRNA landscape in breast cancer. Nature. 2013; 497(7449): 378–382.
    CrossRefPubMed
  11. Ha TY. MicroRNAs in Human Diseases: From Cancer to Cardiovascular Disease. Immune Netw. 2011; 11(3): 135–154.
    CrossRefPubMed
  12. Irshad S, Ellis P, Tutt A. Molecular heterogeneity of triple-negative breast cancer and its clinical implications. Curr Opin Oncol. 2011; 23(6): 566–577.
    CrossRefPubMed
  13. Hsu YH, Yao J, Chan LC, et al. Definition of PKC-α, CDK6, and MET as therapeutic targets in triple-negative breast cancer. Cancer Res. 2014; 74(17): 4822–4835.
    CrossRefPubMed
  14. Avery-Kiejda KA, Braye SG, Mathe A, et al. Decreased expression of key tumour suppressor microRNAs is associated with lymph node metastases in triple negative breast cancer. BMC Cancer. 2014; 14: 51.
    CrossRefPubMed
  15. Matamala N, Vargas MT, González-Cámpora R, et al. MicroRNA deregulation in triple negative breast cancer reveals a role of miR-498 in regulating BRCA1 expression. Oncotarget. 2016; 7(15): 20068–20079.
    CrossRefPubMed
  16. Andersen CL, Jensen JL, Ørntoft TF. Normalization of real-time quantitative reverse transcription-PCR data: a model-based variance estimation approach to identify genes suited for normalization, applied to bladder and colon cancer data sets. Cancer Res. 2004; 64(15): 5245–5250.
    CrossRefPubMed
  17. Chou CH, Chang NW, Shrestha S, et al. miRTarBase 2016: updates to the experimentally validated miRNA-target interactions database. Nucleic Acids Res. 2016; 44(D1): D239–D247.
    CrossRefPubMed
  18. Wang F, Zhong S, Zhang H, et al. Prognostic Value of MicroRNA-182 in Cancers: A Meta-Analysis. Dis Markers. 2015; 2015: 482146.
    CrossRefPubMed
  19. Medimegh I, Omrane I, Privat M, et al. MicroRNAs expression in triple negative vs non triple negative breast cancer in Tunisia: interaction with clinical outcome. PLoS One. 2014; 9(11): e111877.
    CrossRefPubMed
  20. Wei Q, Lei R, Hu G. Roles of miR-182 in sensory organ development and cancer. Thorac Cancer. 2015; 6(1): 2–9.
    CrossRefPubMed
  21. Moskwa P, Buffa FM, Pan Y, et al. miR-182-mediated downregulation of BRCA1 impacts DNA repair and sensitivity to PARP inhibitors. Mol Cell. 2011; 41(2): 210–220.
    CrossRefPubMed
  22. Severson TM, Peeters J, Majewski I, et al. BRCA1-like signature in triple negative breast cancer: Molecular and clinical characterization reveals subgroups with therapeutic potential. Mol Oncol. 2015; 9(8): 1528–1538.
    CrossRefPubMed
  23. de Ruijter TC, Veeck J, de Hoon JPJ, et al. Characteristics of triple-negative breast cancer. J Cancer Res Clin Oncol. 2011; 137(2): 183–192.
    CrossRefPubMed
  24. Krishnan K, Steptoe AL, Martin HC, et al. MicroRNA-182-5p targets a network of genes involved in DNA repair. RNA. 2013; 19(2): 230–242.
    CrossRefPubMed
  25. Arigoni M, Barutello G, Riccardo F, et al. miR-135b coordinates progression of ErbB2-driven mammary carcinomas through suppression of MID1 and MTCH2. Am J Pathol. 2013; 182(6): 2058–2070.
    CrossRefPubMed
  26. Muñoz-Rodríguez JL, Vrba L, Futscher BW, et al. Differentially expressed microRNAs in postpartum breast cancer in Hispanic women. PLoS One. 2015; 10(4): e0124340.
    CrossRefPubMed
  27. Hua K, Jin J, Zhao J, et al. miR-135b, upregulated in breast cancer, promotes cell growth and disrupts the cell cycle by regulating LATS2. Int J Oncol. 2016; 48(5): 1997–2006.
    CrossRefPubMed
  28. Hao Y, Yang J, Yin S, et al. The synergistic regulation of VEGF-mediated angiogenesis through miR-190 and target genes. RNA. 2014; 20(8): 1328–1336.
    CrossRefPubMed
  29. Chu HW, Cheng CW, Chou WC, et al. A novel estrogen receptor-microRNA 190a-PAR-1-pathway regulates breast cancer progression, a finding initially suggested by genome-wide analysis of loci associated with lymph-node metastasis. Hum Mol Genet. 2014; 23(2): 355–367.
    CrossRefPubMed
  30. Yang J, Lan H, Huang X, et al. MicroRNA-126 inhibits tumor cell growth and its expression level correlates with poor survival in non-small cell lung cancer patients. PLoS One. 2012; 7(8): e42978.
    CrossRefPubMed
  31. Wang CZ, Yuan P, Li Y. MiR-126 regulated breast cancer cell invasion by targeting ADAM9. Int J Clin Exp Pathol. 2015; 8(6): 6547–6553.
    PubMed
  32. Tavazoie SF, Alarcón C, Oskarsson T, et al. Endogenous human microRNAs that suppress breast cancer metastasis. Nature. 2008; 451(7175): 147–152.
    CrossRefPubMed
  33. Liu Xi, Sempere LF, Ouyang H, et al. MicroRNA-31 functions as an oncogenic microRNA in mouse and human lung cancer cells by repressing specific tumor suppressors. J Clin Invest. 2010; 120(4): 1298–1309.
    CrossRefPubMed
  34. Zhao H, Liu S, Wang G, et al. Expression of miR-136 is associated with the primary cisplatin resistance of human epithelial ovarian cancer. Oncol Rep. 2015; 33(2): 591–598.
    CrossRefPubMed
  35. Yan M, Li X, Tong D, et al. miR-136 suppresses tumor invasion and metastasis by targeting RASAL2 in triple-negative breast cancer. Oncol Rep. 2016; 36(1): 65–71.
    CrossRefPubMed

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