# The Multifaceted Role of Autophagy in Nasopharyngeal Carcinoma: Translational Perspectives on Pathogenesis, Biomarkers, Treatment Resistance, and Emerging Therapies

**Authors:** Abdul L. Shakerdi, Emma Finnegan, Yin-Yin Sheng, Graham P. Pidgeon

PMC · DOI: 10.3390/cancers17152577 · Cancers · 2025-08-05

## TL;DR

This review explores how autophagy, a cell recycling process, can both help and hinder nasopharyngeal carcinoma, offering insights into new treatment strategies.

## Contribution

The paper provides a comprehensive overview of autophagy's dual role in NPC pathogenesis and treatment resistance, highlighting potential therapeutic strategies.

## Key findings

- Autophagy contributes to both tumor suppression and progression in nasopharyngeal carcinoma.
- Autophagy-related genes like SQSTM1, Beclin-1, and AURKA may serve as biomarkers for prognosis and therapy.
- Modulating autophagy through inhibitors, RNA interventions, and natural compounds is being explored for treatment.

## Abstract

Nasopharyngeal carcinoma (NPC) is a type of cancer that forms in the upper part of the throat, behind the nose. Although rare in most parts of the world, it is much more common in certain regions such as Southeast Asia. This review focuses on a process called autophagy, a natural mechanism cells use to break down and recycle their components. In NPC, autophagy plays a complex role. It can help cancer cells survive under stress such as chemotherapy, but it can also trigger cell death under certain conditions. Understanding how autophagy is regulated in NPC may reveal new ways to improve treatment outcomes. We summarise the current knowledge about autophagy’s dual role in NPC progression and resistance to therapy and explore potential strategies to target autophagy in future treatments. This article is intended to help researchers and clinicians better understand how manipulating autophagy could contribute to more effective NPC therapies.

Background: Nasopharyngeal carcinoma (NPC) is an epithelial malignancy arising from the nasopharyngeal mucosa. Despite treatment advances such as the use of intensity-modulated radiotherapy and immune checkpoint inhibitors, resistance remains a significant clinical challenge. Many tumours are also diagnosed at an advanced stage associated with poor prognosis. Objective: This review aims to explore the biological roles of autophagy in NPC, primarily highlighting its involvement in disease pathogenesis and treatment resistance. Methods: We performed a review of the recent literature examining the role of autophagy-related pathways in NPC pathogenesis, biomarker discovery, and therapeutic targeting. Results: Autophagy plays a dual role in NPC as it contributes to both tumour suppression and progression. It is involved in tumour initiation, metastasis, immune modulation, and treatment resistance. Autophagy-related genes such as SQSTM1, Beclin-1, and AURKA may serve as prognostic and therapeutic biomarkers. Various strategies are being investigated for their role to modulate autophagy using pharmacologic inhibitors, RNA interventions, and natural compounds. Conclusions: Further research into autophagy’s context-dependent roles in NPC may inform the development of personalised therapies and allow progress in translational and precision oncology.

## Linked entities

- **Genes:** SQSTM1 (sequestosome 1) [NCBI Gene 8878], BECN1 (beclin 1) [NCBI Gene 8678], AURKA (aurora kinase A) [NCBI Gene 6790]
- **Diseases:** nasopharyngeal carcinoma (MONDO:0015459)

## Full-text entities

- **Genes:** BECN1 (beclin 1) [NCBI Gene 8678] {aka ATG6, VPS30, beclin1}, SQSTM1 (sequestosome 1) [NCBI Gene 8878] {aka A170, DMRV, EBIAP, FTDALS3, NADGP, OSIL}, AURKA (aurora kinase A) [NCBI Gene 6790] {aka AIK, ARK1, AURA, BTAK, PPP1R47, STK15}
- **Diseases:** tumour (MESH:D009369), NPC (MESH:D000077274), epithelial malignancy (MESH:D002277), metastasis (MESH:D009362)

## Full text

_Full body text omitted from this summary view._ Fetch the complete paper as Markdown: https://tomesphere.com/paper/PMC12346892/full.md

## Figures

4 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12346892/full.md

## References

111 references — full list in the complete paper: https://tomesphere.com/paper/PMC12346892/full.md

---
Source: https://tomesphere.com/paper/PMC12346892