Identification of IL11RA and MELK amplification in gastric cancer by comprehensive genomic profiling of gastric cancer cell lines

被引:17
作者
Calcagno, Danielle Queiroz [1 ,2 ]
Takeno, Sylvia Santomi [1 ,3 ]
Gigek, Carolina Oliveira [1 ,4 ]
Leal, Mariana Ferreira [1 ,5 ]
Wisnieski, Fernanda [1 ]
Chen, Elizabeth Suchi [1 ]
Thomaz Araujo, Taissa Maira [2 ]
Lima, Eleonidas Moura [3 ]
Melaragno, Maria Isabel [1 ]
Demachki, Samia [2 ]
Assumpcao, Paulo Pimentel [2 ]
Burbano, Rommel Rodriguez [2 ]
Smith, Marilia Cardoso [1 ]
机构
[1] Univ Fed Sao Paulo, Dept Morfol & Genet, Disciplina Genet, BR-04021001 Sao Paulo, SP, Brazil
[2] Hosp Univ Joao Barros Barreto, Nucleo Pesquisas Oncol, Av Mundurucus 4487,1 Piso Unacon, BR-66073000 Belem, PA, Brazil
[3] Univ Fed Paraiba, Dept Biol Mol, BR-58051900 Joao Pessoa, Paraiba, Brazil
[4] Univ Fed Sao Paulo, Disciplina Gastroenterol Cirurg, BR-04021001 Sao Paulo, SP, Brazil
[5] Univ Fed Sao Paulo, Dept Ortopedia & Traumatol, BR-04021001 Sao Paulo, SP, Brazil
基金
巴西圣保罗研究基金会;
关键词
IL11RA; Gastric cancer; Genomic profiling; MELK; 9p13.3; INTERLEUKIN-11; RECEPTOR-ALPHA; CONVENTIONAL CYTOGENETIC CHARACTERIZATION; COPY NUMBER ALTERATIONS; C-MYC AMPLIFICATION; HUMAN BREAST-CANCER; GENETIC ALTERATIONS; PROSTATE-CANCER; INCREASED EXPRESSION; THERAPEUTIC TARGET; NORTHERN BRAZIL;
D O I
10.3748/wjg.v22.i43.9506
中图分类号
R57 [消化系及腹部疾病];
学科分类号
摘要
AIM To identify common copy number alterations on gastric cancer cell lines. METHODS Four gastric cancer cell lines (ACP02, ACP03, AGP01 and PG100) underwent chromosomal comparative genome hybridization and array comparative genome hybridization. We also confirmed the results by fluorescence in situ hybridization analysis using the bacterial artificial chromosome clone and quantitative real time PCR analysis. RESULTS The amplification of 9p13.3 was detected in all cell lines by both methodologies. An increase in the copy number of 9p13.3 was also confirmed by fluorescence in situ hybridization analysis. Moreover, the interleukin 11 receptor alpha (IL11RA) and maternal embryonic leucine zipper kinase (MELK) genes, which are present in the 9p13.3 amplicon, revealed gains of the MELK gene in all the cell lines studied. Additionally, a gain in the copy number of IL11RA and MELK was observed in 19.1% (13/68) and 55.9% (38/68) of primary gastric adenocarcinoma samples, respectively. CONCLUSION The characterization of a small gain region at 9p13.3 in gastric cancer cell lines and primary gastric adenocarcinoma samples has revealed MELK as a candidate target gene that is possibly related to the development of gastric cancer.
引用
收藏
页码:9506 / 9514
页数:9
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