Link to the University of Pittsburgh Homepage
Link to the University Library System Homepage Link to the Contact Us Form
D-Scholarship @ Pitt Banner and Links to Homepage

Gene expression analysis indicates divergent mechanisms in DEN-induced carcinogenesis in wild type and bid-deficient livers

Yu, C and Yan, S and Khambu, B and Chen, X and Dong, Z and Luo, J and Michalopoulos, GK and Wu, S and Yin, XM (2016) Gene expression analysis indicates divergent mechanisms in DEN-induced carcinogenesis in wild type and bid-deficient livers. PLoS ONE, 11 (5).

[img]
Preview
 PDF
Published Version
Available under License : See the attached license file.
Download (1MB)
[img] Plain Text (licence)
Available under License : See the attached license file.
Download (1kB)

Abstract

© 2016 Yu et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Bid is a Bcl-2 family protein. In addition to its pro-apoptosis function, Bid can also promote cell proliferation, maintain S phase checkpoint, and facilitate inflammasome activation. Bid plays important roles in tissue injury and regeneration, hematopoietic homeostasis, and tumorigenesis. Bid participates in hepatic carcinogenesis but the mechanism is not fully understood. Deletion of Bid resulted in diminished tumor burden and delayed tumor progression in a liver cancer model. In order to better understand the Bid-regulated events during hepatic carcinogenesis we performed gene expression analysis in wild type and bid-deficient mice treated with a hepatic carcinogen, diethylnitrosamine. We found that deletion of Bid caused significantly fewer alterations in gene expression in terms of the number of genes affected and the number of pathways affected. In addition, the expression profiles were remarkably different. In the wild type mice, there was a significant increase in the expression of growth regulation-related and immune/inflammation response-related genes, and a significant decrease in the expression of metabolism-related genes, both of which were diminished in bid-deficient livers. These data suggest that Bid could promote hepatic carcinogenesis via growth control and inflammation-mediated events.

Share

Citation/Export:
Social Networking:
Share |

Details

Item Type: Article
Status: Published
Creators/Authors:
CreatorsEmailPitt UsernameORCID
Yu, C
Yan, S
Khambu, B
Chen, X
Dong, Z
Luo, JLUOJH@pitt.eduLUOJH
Michalopoulos, GKmichal@pitt.eduMICHAL
Wu, S
Yin, XM
Contributors:
ContributionContributors NameEmailPitt UsernameORCID
EditorGao, AllenUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Date: 1 May 2016
Date Type: Publication
Access Restriction: No restriction; Release the ETD for access worldwide immediately.
Journal or Publication Title: PLoS ONE
Volume: 11
Number: 5
DOI or Unique Handle: 10.1371/journal.pone.0155211
Institution: University of Pittsburgh
Schools and Programs: School of Medicine > Pathology
Refereed: Yes
Date Deposited: 22 Dec 2016 16:02
Last Modified: 05 Feb 2019 16:55
URI: http://d-scholarship.pitt.edu/id/eprint/28230

Metrics

Monthly Views for the past 3 years

Plum Analytics

Altmetric.com

Actions (login required)

View Item View Item