PMID- 38317842
OWN - NLM
STAT- MEDLINE
DCOM- 20240207
LR  - 20240207
IS  - 2167-8359 (Electronic)
IS  - 2167-8359 (Linking)
VI  - 12
DP  - 2024
TI  - Novel application of the ferroptosis-related genes risk model associated with 
      disulfidptosis in hepatocellular carcinoma prognosis and immune infiltration.
PG  - e16819
LID - 10.7717/peerj.16819 [doi]
LID - e16819
AB  - Hepatocellular carcinoma (HCC) stands as the prevailing manifestation of primary 
      liver cancer and continues to pose a formidable challenge to human well-being and 
      longevity, owing to its elevated incidence and mortality rates. Nevertheless, the 
      quest for reliable predictive biomarkers for HCC remains ongoing. Recent research 
      has demonstrated a close correlation between ferroptosis and disulfidptosis, two 
      cellular processes, and cancer prognosis, suggesting their potential as 
      predictive factors for HCC. In this study, we employed a combination of 
      bioinformatics algorithms and machine learning techniques, leveraging RNA 
      sequencing data, mutation profiles, and clinical data from HCC samples in The 
      Cancer Genome Atlas (TCGA), Gene Expression Omnibus (GEO), and the International 
      Cancer Genome Consortium (ICGC) databases, to develop a risk prognosis model 
      based on genes associated with ferroptosis and disulfidptosis. We conducted an 
      unsupervised clustering analysis, calculating a risk score (RS) to predict the 
      prognosis of HCC using these genes. Clustering analysis revealed two distinct HCC 
      clusters, each characterized by significantly different prognostic and immune 
      features. The median RS stratified HCC samples in the TCGA, GEO, and ICGC cohorts 
      into high-and low-risk groups. Importantly, RS emerged as an independent 
      prognostic factor in all three cohorts, with the high-risk group demonstrating 
      poorer prognosis and a more active immunosuppressive microenvironment. 
      Additionally, the high-risk group exhibited higher expression levels of tumor 
      mutation burden (TMB), immune checkpoints (ICs), and human leukocyte antigen 
      (HLA), suggesting a heightened responsiveness to immunotherapy. A cancer stem 
      cell infiltration analysis revealed a higher similarity between tumor cells and 
      stem cells in the high-risk group. Furthermore, drug sensitivity analysis 
      highlighted significant differences in response to antitumor drugs between the 
      two risk groups. In summary, our risk prognostic model, constructed based on 
      ferroptosis-related genes associated with disulfidptosis, effectively predicts 
      HCC prognosis. These findings hold potential implications for patient 
      stratification and clinical decision-making, offering valuable theoretical 
      insights in this field.
CI  - (c) 2024 Wei et al.
FAU - Wei, Jiayan
AU  - Wei J
AD  - Department of Oncology, Renmin Hospital of Wuhan University, Wuhan, Hubei, China.
FAU - Wang, Jinsong
AU  - Wang J
AD  - Department of Oncology, Renmin Hospital of Wuhan University, Wuhan, Hubei, China.
FAU - Chen, Xinyi
AU  - Chen X
AD  - Department of Oncology, Renmin Hospital of Wuhan University, Wuhan, Hubei, China.
FAU - Zhang, Li
AU  - Zhang L
AD  - Basic Medical Sciences, Wuhan University School of Basic Medical Sciences, Wuhan, 
      Hubei, China.
FAU - Peng, Min
AU  - Peng M
AD  - Department of Oncology, Renmin Hospital of Wuhan University, Wuhan, Hubei, China.
LA  - eng
SI  - figshare/10.6084/m9.figshare.24971169.v1
PT  - Journal Article
DEP - 20240202
PL  - United States
TA  - PeerJ
JT  - PeerJ
JID - 101603425
SB  - IM
MH  - Humans
MH  - *Carcinoma, Hepatocellular/genetics
MH  - *Ferroptosis/genetics
MH  - *Liver Neoplasms/genetics
MH  - Algorithms
MH  - Clinical Decision-Making
MH  - Tumor Microenvironment
PMC - PMC10840499
OTO - NOTNLM
OT  - Disulfidptosis
OT  - Ferroptosis
OT  - HCC
OT  - Prognosis model
OT  - Tumor microenvironment
COIS- The authors declare that they have no competing interests.
EDAT- 2024/02/06 06:42
MHDA- 2024/02/07 06:43
PMCR- 2024/02/02
CRDT- 2024/02/06 03:48
PHST- 2023/07/13 00:00 [received]
PHST- 2023/12/31 00:00 [accepted]
PHST- 2024/02/07 06:43 [medline]
PHST- 2024/02/06 06:42 [pubmed]
PHST- 2024/02/06 03:48 [entrez]
PHST- 2024/02/02 00:00 [pmc-release]
AID - 16819 [pii]
AID - 10.7717/peerj.16819 [doi]
PST - epublish
SO  - PeerJ. 2024 Feb 2;12:e16819. doi: 10.7717/peerj.16819. eCollection 2024.