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Derlin-1 functions as a growth promoter in breast cancer

Authors
  • Liu, Yansong1
  • Wang, Ziming2
  • Liu, Handong3
  • Wang, Xin4
  • Zhang, Zhonghua5
  • Xiao, Bin6
  • An, Baoming7
  • Zhang, Jun8
  • 1 Shandong Cancer Hospital, 440 Jiyan Road, Shandong , (China)
  • 2 The Second Children and Women’s Healthcare of Jinan City, 12 Fengcheng West Road, Laiwu District , (China)
  • 3 Jinan Integrated Traditional Chinese and Western Medicine Hospital, 8 Wanyuan East Road, Laiwu District, Shandong , (China)
  • 4 Yinan People’s Hospital, 50 Lishan Road, Shandong , (China)
  • 5 Dongping Country People’s Hospital, Shandong , (China)
  • 6 Shanxian Hygeia Hospital, West Lake Road, Shandong , (China)
  • 7 Wulian People’s Hospital, 50 Limin Road, Shandong , (China)
  • 8 Zhangqiu Hospital of Chinese Medicine, 1463 Mingshui Road, Zhangqiu District, Shandong , (China)
Type
Published Article
Journal
Biological Chemistry
Publisher
Walter de Gruyter GmbH
Publication Date
Nov 14, 2019
Volume
401
Issue
3
Pages
377–387
Identifiers
DOI: 10.1515/hsz-2018-0442
Source
De Gruyter
Keywords
License
Yellow

Abstract

Breast cancer is one of the most common malignant tumors in women. Derlin-1 has been found to be overexpressed in several human cancers in addition to playing an important role in tumor processes; however, the expression patterns and functions of Derlin-1 in human breast cancer are not fully understood. In this study, we found that Derlin-1 overexpression was higher in breast cancer compared to normal samples through TCGA and GTEx database analyses. Kaplan-Meier plotter analysis showed that Derlin-1 was a predicting factor for patient prognosis. Derlin-1 expression was significantly up-regulated in breast cancer tissues (18/30, 60.00%) compared to corresponding paracancerous tissue (9/30, 30.00%, p < 0.05) as detected by immunohistochemistry, and the expression of Derlin-1 was correlated to pathological grading. siRNA interference of Derlin-1 inhibited cell proliferation, which is associated with the promotion of apoptosis and migration. Derlin-1 knockdown suppressed the protein levels of p-AKT and Cyclin D1 while up-regulating Caspase3 and Bax. GEPIA database analysis showed that MTDH and ATAD2 were downstream target genes, and the expression of MTDH and was suppressed in Derlin-1 knockdown cells. Taken together, our results demonstrated ATAD2 that Derlin-1 is overexpressed in breast cancer and promoted a malignant phenotype through the AKT signaling pathway.

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