Please use this identifier to cite or link to this item: http://hdl.handle.net/10553/119577
Title: SOCS2 protects against chemical-induced hepatocellular carcinoma progression by modulating inflammation and cell proliferation in the liver
Authors: Cabrera Galván, Juan José 
Araujo Ruano, Eduardo
De Mirecki Garrido, Mercedes 
Pérez Rodríguez, David
Guerra Hernández, Carlos Borja 
Aranda Tavío, Haidée Magdalena 
Guerra Rodríguez, Miguel Alfonso 
Brito Casillas, Yeray 
Melián Limiñana, Carlos 
Martínez Martín, María Soledad 
Fernández Pérez, Leandro Fco 
Recio Cruz, Carlota Pilar 
UNESCO Clasification: 32 Ciencias médicas
3209 Farmacología
Keywords: Hepatocellular carcinoma
SOCS2
STAT
Inflammation
Therapeutic target, et al
Issue Date: 2022
Journal: Biomedicine and Pharmacotherapy 
Abstract: Hepatocellular carcinoma (HCC) is one of the most prevalent and lethal cancers worldwide, but the precise intracellular mechanisms underlying the progression of this inflammation associated cancer are not well established. SOCS2 protein plays an important role in the carcinogenesis of different tumors by regulating cytokine signalling through the JAK/STAT axis. However, its role in HCC is unclear. Here, we investigate the role of SOCS2 in HCC progression and its potential as HCC biomarker. The effects of SOCS2 in HCC progression were evaluated in an experimental model of diethylnitrosamine (DEN)-induced HCC in C57BL/6 and SOCS2 deficient mice, in cultured hepatic cells, and in liver samples from HCC patients. Mice lacking SOCS2 showed higher liver tumor burden with increased malignancy grade, inflammation, fibrosis, and proliferation than their controls. Protein and gene expression analysis reported higher pSTAT5 and pSTAT3 activation, upregulation of different proteins involved in survival and proliferation, and increased levels of proinflammatory and pro-tumoral mediators in the absence of SOCS2. Clinically relevant, downregulated expression of SOCS2 was found in neoplasia from HCC patients compared to healthy liver tissue, correlating with the malignancy grade. In summary, our data show that lack of SOCS2 increases susceptibility to chemical-induced HCC and suggest the tumor suppressor role of this protein by regulating the oncogenic and inflammatory responses mediated by STAT5 and STAT3 in the liver. Hence, SOCS2 emerges as an attractive target molecule and potential biomarker to deepen in the study of HCC treatment.
URI: http://hdl.handle.net/10553/119577
ISSN: 0753-3322
DOI: 10.1016/j.biopha.2022.114060
Source: Biomedicine & Pharmacotherapy [ISSN 0753-3322], v. 157, 114060, (Enero 2023)
Appears in Collections:Artículos
Adobe PDF (22,29 MB)
Show full item record

SCOPUSTM   
Citations

11
checked on Oct 27, 2024

WEB OF SCIENCETM
Citations

11
checked on Oct 27, 2024

Page view(s)

149
checked on May 25, 2024

Download(s)

60
checked on May 25, 2024

Google ScholarTM

Check

Altmetric


Share



Export metadata



Items in accedaCRIS are protected by copyright, with all rights reserved, unless otherwise indicated.