Research Papers:

RNA sequencing analyses reveal novel differentially expressed genes and pathways in pancreatic cancer

Yixiang Mao, Jianjun Shen, Yue Lu, Kevin Lin, Huamin Wang, Yanan Li, Ping Chang, Mary G. Walker and Donghui Li _

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Oncotarget. 2017; 8:42537-42547. https://doi.org/10.18632/oncotarget.16451

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Yixiang Mao1,2,5, Jianjun Shen4, Yue Lu4, Kevin Lin4, Huamin Wang3, Yanan Li2, Ping Chang2, Mary G. Walker4 and Donghui Li2

1Department of Oncology, The First Affiliated Hospital of Soochow University, Suzhou 215007, China

2Department of Gastrointestinal Medical Oncology, The University of Texas MD Anderson Cancer Center, Houston, Texas 77030, USA

3Department of Pathology and Department of Translational Molecular Pathology, The University of Texas MD Anderson Cancer Center, Houston, Texas 77030, USA

4Department of Epigenetics and Molecular Carcinogenesis, The University of Texas MD Anderson Cancer Center, Smithville, Texas 78957, USA

5Department of Medical Oncology, Fudan University Shanghai Cancer Center, Shanghai 200032, China

Correspondence to:

Donghui Li, email: [email protected]

Yixiang Mao, email: [email protected]

Keywords: pancreatic cancer, RNA sequencing, transcriptome, pathway analysis

Received: June 03, 2016    Accepted: February 27, 2017    Published: March 22, 2017


Gene expression microarrays have identified many tumor markers and therapeutic targets for pancreatic ductal adenocarcinoma (PDAC). However, microarray profilings have limited sensitivity and are prone to cross-hybridization between homologous DNA fragments. Here, we perform a transcriptome analysis of paired tumor and adjacent benign pancreatic tissues from 10 patients who underwent resection for PDAC. We identify a total of 2736 differentially expressed genes (DEGs) with false discovery rate less than 0.05, including 1554 upregulated, 1182 downregulated, and 6 microRNAs (miR-614, miR-217, miR-27b, miR-4451, miR-3609, and miR-612). Overexpression of five DEGs, i.e. KRT16, HOXA10, CDX1, SI, and SERPINB5 in tumors is confirmed by RT-PCR in 20 additional tissues. Overexpression of KRT16 in PDAC is also verified on protein level. In addition, top canonical pathways such as granulocyte adhesion and diapedesis pathway have been identified. Our study represents a comprehensive characterization of the PDAC transcriptome and provides insight to the mechanisms of pancreatic carcinogenesis and potential biomarkers and novel therapeutic targets for pancreatic cancer.

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