Affordable Access

deepdyve-link
Publisher Website

Sec62 promotes pro-angiogenesis of hepatocellular carcinoma cells under hypoxia.

Authors
  • Meng, Yongbin1
  • Zhao, Hetong1
  • Zhao, Zhihao1
  • Yin, Zifei1
  • Chen, Zhe1
  • Du, Juan2
  • 1 Department of Traditional Chinese Medicine, Changhai Hospital, Naval Medical University, Shanghai, China. , (China)
  • 2 Department of Traditional Chinese Medicine, Changhai Hospital, Naval Medical University, Shanghai, China. [email protected] , (China)
Type
Published Article
Journal
Cell Biochemistry and Biophysics
Publisher
Springer-Verlag
Publication Date
Dec 01, 2021
Volume
79
Issue
4
Pages
747–755
Identifiers
DOI: 10.1007/s12013-021-01008-6
PMID: 34120320
Source
Medline
Keywords
Language
English
License
Unknown

Abstract

This study aimed to investigate the underlying molecular pathogenic mechanism of Sec62 in hepatocellular carcinoma (HCC). Microarray analysis was conducted to profile the global gene expression in the HCC cell line Huh7 cells transfected with Sec62high vs. NC and Sec62low vs. NC. Ingenuity pathway analysis and gene set enrichment analysis were used to perform Sec62-related signaling pathway analysis from screened differentially expressed genes (DEGs). A protein-protein interaction network was constructed. Experimental validation of the expression of key DEGs was conducted. Hypoxia-induced tube formation was undertaken to investigate the role of Sec62 in angiogenesis. A total of 74 intersected DEGs were identified from Huh7 cells with Sec62high vs. NC and Sec62low vs. NC. Among them, 65 DEGs were correlated with the expression of Sec62. The P53 signaling pathway was found to be enriched in Huh7 cells with Sec62high vs. NC, while the acute phase response signaling pathway was enriched in Huh7 cells with Sec62low vs. NC. DEGs, such as serine protease inhibitor E (SERPINE) and tumor necrosis factor receptor superfamily, member 11B (TNFRSF11B), were not only identified as the lead genes of these enriched pathways, but were also found to be closely related to Sec62. Moreover, knockdown of Sec62 decreased the expression of SERPINE1 (plasminogen activator inhibitor type 1 (PAI-1)) and TNFRSF11B, whereas overexpression of Sec62 had the opposite effects. In addition, knockdown of Sec62 inhibited hypoxia-induced tube formation via PAI-1. Sec62 promoted pro-angiogenesis of HCC under hypoxia by regulating PAI-1, and it may be a crucial angiogenic switch in HCC. © 2021. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.

Report this publication

Statistics

Seen <100 times