Identifying and evaluating a disulfidptosis-related gene signature to predict prognosis in colorectal adenocarcinoma patients

  • 0Department of General Surgery, The Second Affiliated Hospital of Soochow University, Suzhou, China.

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Summary

This summary is machine-generated.

This study introduces a new prognostic model for colon adenocarcinoma (COAD) using 20 disulfidptosis-related genes (DRGs). The model predicts patient outcomes and highlights POU4F1

Area Of Science

  • Oncology
  • Cell Death Research
  • Genomics

Background

  • Disulfidptosis, a regulated cell death, is observed in cancers with high SLC7A11 expression.
  • Its role in colon adenocarcinoma (COAD) remains under-explored.
  • Understanding disulfidptosis in COAD is crucial for developing novel therapeutic strategies.

Purpose Of The Study

  • To develop and validate a prognostic model for COAD based on disulfidptosis-related genes (DRGs).
  • To investigate the correlation between the risk score and cancer-related biological processes, immune infiltration, and gene expression.
  • To elucidate the specific role of POU4F1 in COAD progression and disulfidptosis.

Main Methods

  • Utilized LASSO and Cox regression analyses to build a prognostic model from 20 DRGs.
  • Developed a nomogram to assess the model's robustness and clinical applicability.
  • Performed correlation, enrichment, and in vitro assays to analyze gene functions and cellular responses.

Main Results

  • A validated DRG-based prognostic model for COAD patients was established.
  • The risk score correlated with key cancer pathways, immune cell infiltration, and oncogene expression.
  • POU4F1 was identified as an oncogene in COAD, promoting proliferation and migration, and potentially regulating disulfidptosis.

Conclusions

  • The developed DRG-based model offers a valuable tool for predicting COAD patient prognosis.
  • POU4F1 plays a significant role in COAD progression and may be a therapeutic target.
  • This research sheds light on the role of disulfidptosis in COAD and its relationship with oncogenic pathways.