2. Academic Validation
  3. High expression of diffuse panbronchiolitis critical region 1 gene promotes cell proliferation, migration and invasion in pancreatic ductal adenocarcinoma

High expression of diffuse panbronchiolitis critical region 1 gene promotes cell proliferation, migration and invasion in pancreatic ductal adenocarcinoma

  • Biochem Biophys Res Commun. 2018 Jan 8;495(2):1908-1914. doi: 10.1016/j.bbrc.2017.12.031.
Jiayi Yan 1,  Guanghui Chen 2,  Xuesong Zhao 1,  Fangying Chen 1,  Ting Wang 3,  Fei Miao 4
Affiliations

Affiliations

  • 1 Department of Radiology, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, 197 Ruijin Er Road, Shanghai 200025, China.
  • 2 Department of Bone Tumor Surgery, Changzheng Hospital, Second Military Medical University, 415 Fengyang Road, Shanghai 200003, China.
  • 3 Department of Bone Tumor Surgery, Changzheng Hospital, Second Military Medical University, 415 Fengyang Road, Shanghai 200003, China. Electronic address: [email protected].
  • 4 Department of Radiology, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, 197 Ruijin Er Road, Shanghai 200025, China. Electronic address: [email protected].
PMID: 29242154 DOI: 10.1016/j.bbrc.2017.12.031
Abstract

Diffuse panbronchiolitis critical region 1 (DPCR1) is located in the major histocompatibility complex (MHC) class I. It was reported to be downregulated in invasive pituitary adenoma compared with that in non-invasive tumors, but upregulated in the precursor of gastric carcinogenesis. However, the direct effect of DPCR1 on Cancer cells has rarely been reported, and the role DPCR1 in pancreatic ductal adenocarcinoma (PDAC) remains unclear. The clinical sample validation and public data analysis of the present study demonstrated that DPCR1 was upregulated markedly in PDAC and this high expression was negatively correlated with the patient prognosis. Functionally, knocking down DPCR1 in PDAC cell lines inhibited cell proliferation, migration and invasion in vitro. Tumor xenograft experiments further showed that suppression of DPCR1 inhibited tumor growth in vivo. In addition, the results of RNA deep sequencing and qRT-PCR assay showed that DPCR1 participated in PADC progression by regulating nuclear factor-kappa B signaling pathway, suggesting that it might be a novel oncogene in tumor progression and a potential therapeutic target in PDAC as well.

Keywords

Cell proliferation; DPCR1; Invasion; Migration; NF-κB signaling pathway; PDAC.

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