Multiomics Analysis of Disulfidptosis Patterns and Integrated Machine Learning to Predict Immunotherapy Response in Lung Adenocarcinoma

Junzhi Liu ¹, Huimin Li ², Nannan Zhang ¹

⁰Department of Otorhinolaryngology, Tianjin Medical University General Hospital, Tianjin, 300052, China.

Current Medicinal Chemistry +

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April 30, 2024

View abstract on PubMed

Summary

Disulfidptosis, a cell death pathway, impacts lung adenocarcinoma (LUAD) tumor immunity. A new risk model predicts immunotherapy response and identifies NAPSA as a potential therapeutic target in LUAD.

Area Of Science

Oncology
Cell Death Mechanisms
Immunotherapy

Background

Disulfidptosis is a cell death mechanism linked to cellular damage.
Understanding disulfidptosis in lung adenocarcinoma (LUAD) offers new insights into tumor dynamics and treatment strategies.

Purpose Of The Study

To investigate the impact of disulfidptosis on the tumor immune microenvironment in LUAD.
To develop a prognostic model for predicting immunotherapy response in LUAD patients based on disulfidptosis-related genes.

Main Methods

Pan-cancer transcriptomics analysis of disulfidptosis-related genes.
Multi-omics data analysis of LUAD cohorts from TCGA.
Machine learning model construction for prognosis and immunotherapy prediction.
Single-cell transcriptome analysis to assess tumor microenvironment impact.
In vitro validation of gene functions.

Main Results

Disulfidptosis genes show significant expression and prognostic value in cancers, including LUAD.
Two distinct disulfidptosis subtypes identified in LUAD with different prognoses.
A robust Disulfidptosis Risk Score (DSRS) model developed; lower scores predict better immunotherapy response and survival.
NAPSA identified as a key gene inhibiting LUAD cell proliferation and migration.

Conclusions

An innovative disulfidptosis-based prognostic model for LUAD patients has been developed.
The model accurately predicts survival and therapeutic outcomes, identifying high-risk populations with immunosuppression.
NAPSA shows potential as a therapeutic target to inhibit LUAD cell proliferation and invasion.

Keywords:

Disulfidptosis TCGA database drug response immune microenvironment lung adenocarcinoma. single cell