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601
MATRISOME GENES FROM HEPATITIS B-INDUCED
HEPATOCELLULAR CARCINOMA UNVEILED
Wei Chen1, Romain Desert1, Xiaodong Ge2, Hui Han2, Zhuolun
Song2, Sukanta Das2, Dipti Athavale2, Hong You3 and Natalia
Nieto1, (1)Department of Pathology, University of Illinois at
Chicago, (2)Department of Medicine, University of Illinois
at Chicago, (3)Liver Research Center, Beijing Friendship
Hospital, Capital Medical University, Beijing, China
Background: patients with chronic hepatitis B virus (HBV)
infection are at greater risk of progressing to hepatocellular
carcinoma (HCC) Turnover of the extracellular matrix (ECM)
surrounding the tumor favors HCC onset, progression and
metastasis Since the composition and function of the ECM
in HBV-induced HCC remains unknown, our aim was to
unveil the matrisome genes and their function Methods:
publicly available transcriptomics gene expression profiles
from HBV-induced HCC and other liver diseases were
downloaded from the Gene Expression Omnibus Matrisome
genes were defined according to the MatrisomeDB database.
Using comprehensive bioinformatics tools and databases,
we systematically compared the expression patterns of
matrisome genes between HBV-induced HCC and other
liver diseases We extracted the core matrisome genes
(CMGs) and explored their potential carcinogenic effects
Last, we evaluated the spatial expression mode and the
clinical relevance of the identified CMGs. Results: the overall
expression and dysregulation patterns of matrisome genes
in HBV-induced HCC were largely different from other liver
diseases Differentially expressed matrisome genes that were
notably enriched in the ECM, p53 and immune system-related
pathways were defined as CMGs that could diagnose HBVinduced
HCC from adjacent non-tumor samples with high
AUC values CMGs highly interacted with non-matrisome
genes involved in multiple metabolic pathways and some
cancer-related pathways, including chemical carcinogenesis,
p53 signaling and the cell cycle Among the CMGs, MBL2,
F9, INHBE and PLG were specifically expressed in normal
and cancerous livers Their downregulation was involved
in the activation of cancer-related pathways such as cell
cycle, microRNAs in cancer, viral carcinogenesis, Wnt
signaling and transcriptional misregulation in cancer F9,
IGFBP3, PLG, S100A8, SERPINA5 and SERPINF2 were
associated with HCC progression in HBV-induced but not in
non-HBV-induced HCC samples (except for F9) In addition,
low expression of COLEC11 and MBL2 could predict poor
prognosis, specifically in HBV-induced HCC samples.
Conclusion: this study highlights the overall expression and
function of matrisome genes in HBV-induced HCC CMGs are
highly associated with HCC development, progression and
prognosis in HBV infection. These findings provide a deeper
understanding of the contribution of the matrisome in HCC
and highlights potential therapeutic targets for treating HBVinduced
HCC.
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发表于 2020-10-21 13:01
