An endoplasmic reticulum stress- and Golgi apparatus-related signature reveals immune microenvironment remodeling and MUC16-driven PI3K/AKT activation in lung adenocarcinoma - Report - MDSpire
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A signature associated with endoplasmic reticulum stress and Golgi apparatus dysfunction indicates immune microenvironment alterations and MUC16-mediated PI3K/AKT pathway activation in lung adenocarcinoma

  • By

  • Weihao Zhang

  • Lei Liu

  • Jianwei Liu

  • September 8, 2026

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Clinical Report: EGRG-Based Prognostic Signature in Lung Adenocarcinoma

Overview

A 17-gene prognostic signature related to endoplasmic reticulum stress and Golgi apparatus dysfunction was developed for lung adenocarcinoma (LUAD).

Background

Lung adenocarcinoma (LUAD) is the most common subtype of non-small cell lung cancer, presenting significant clinical challenges due to its heterogeneity and resistance to therapies. Understanding the molecular mechanisms underlying LUAD progression, particularly those involving endoplasmic reticulum stress and Golgi apparatus dysfunction, is crucial.

Data Highlights

FindingDetails
Prognostic Signature17-gene signature developed from 133 differentially expressed genes related to EGRGs.
ValidationPrognostic utility confirmed across independent LUAD cohorts.
Risk CategoriesSignificant differences in tumor microenvironment characteristics and immune infiltration patterns based on risk scores.
MUC16 ExpressionMUC16 was found to be upregulated in LUAD, correlating with poorer patient outcomes.
Mechanistic InsightsMUC16 may activate FAK-mediated PI3K/AKT signaling, contributing to malignant phenotypes.

Key Findings

  • A 17-gene prognostic signature was established based on endoplasmic reticulum stress and Golgi apparatus-related genes.
  • The signature was validated in independent LUAD cohorts, demonstrating prognostic utility.
  • Patients were categorized into risk groups with significant differences in immune microenvironment characteristics.
  • MUC16 was identified as a key gene, with increased expression linked to worse patient outcomes.
  • Functional studies suggest MUC16 facilitates malignant phenotypes via FAK-mediated PI3K/AKT signaling activation.

Clinical Implications

The EGRG-based prognostic signature may assist in risk stratification for LUAD patients. MUC16's role in LUAD progression highlights its potential as a prognostic biomarker.

Conclusion

An EGRG-based prognostic signature for LUAD has been established.

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