An integrative analysis reveals the prognostic value and potential functions of PSMD11 in hepatocellular carcinoma

The global burden of hepatocellular carcinoma (HCC) as a preeminent etiology of cancer‐related mortalities sheds light on the imperative necessity for a more profound comprehension of its fundamental biological mechanisms. In this context, the precise function of the 26S proteasome non‐ATPase regula...

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Published in:Molecular carcinogenesis 2023-09, Vol.62 (9), p.1355-1368
Main Authors: Zhang, Cong, Xu, Tiantian, Ji, Kun, Cao, Shoujin, Cao, Yunbo, Ai, Jing, Jing, Li, Sun, Jun‐Hui
Format: Article
Language:English
Subjects:
bioinformatics analysis
Drug development
Gefitinib
Gene expression
Genomes
Genotypes
Hepatocellular carcinoma
Imatinib
Immunosuppressive agents
Liver cancer
Metastases
Molecular modelling
Mutation rates
prognosis
Proteasome 26S
Proteasomes
PSMD11
TCGA
Therapeutic targets
Tumors
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Summary:The global burden of hepatocellular carcinoma (HCC) as a preeminent etiology of cancer‐related mortalities sheds light on the imperative necessity for a more profound comprehension of its fundamental biological mechanisms. In this context, the precise function of the 26S proteasome non‐ATPase regulatory subunit 11 (PSMD11) in HCC remains equivocal. To address this vital knowledge gap, we interrogated the cancer genome atlas, genotype‐tissue expression, International cancer genome consortium, gene expression omnibus, the cancer cell line encyclopedia, and tumor immune single‐cell hub databases to evaluate the expression pattern of PSMD11, further confirmed by reverse‐transcription quantitative polymerase chain reaction (RT‐qPCR) in LO2, MHCC‐97H, HepG2, and SMMC7721 cell lines. Additionally, we meticulously assessed the clinical significance and prognostic value of PSMD11, while also exploring its potential molecular mechanisms in HCC. Our findings demonstrated that PSMD11 was highly expressed in HCC tissues, correlating with pathologic stage and histologic grade, thereby conferring a poor prognosis. Mechanistically, PSMD11 appears to exert its tumorigenic effects through the modulation of tumor metabolism‐related pathways. Impressively, low PSMD11 expression was associated with increased immune effector cell infiltration, heightened responsiveness to molecular targeted drugs such as dasatinib, erlotinib, gefitinib, and imatinib, as well as reduced somatic mutation rate. Additionally, we demonstrated that PSMD11 might modulate HCC development through intricate interactions with cuproptosis‐related genes ATP7A, DLAT, and PDHA1. Our comprehensive analyses collectively suggest that PSMD11 represents a promising therapeutic target in HCC.
ISSN:0899-1987
1098-2744
DOI:10.1002/mc.23568