Autophagy in Solid Tumors and Inflammation: Mechanisms and Therapies

Autophagy, a fundamental cellular process responsible for the degradation and recycling of damaged organelles and proteins, plays a critical role in maintaining cellular health and homeostasis. This process is intricately linked to both cancer and inflammation, two complex and interrelated conditions that significantly impact human health. In the context of cancer, autophagy can exhibit dual roles. It can act as a tumor suppressor by removing damaged cellular components that could otherwise contribute to tumorigenesis. Conversely, in established cancers, autophagy can promote tumor survival by supporting cancer cells under metabolic stress and therapeutic assault. Similarly, autophagy influences inflammation by regulating the secretion of inflammatory cytokines and the clearing of inflammasomes, thus potentially alleviating or exacerbating inflammatory conditions. The dynamic interactions between autophagy, cancer, and inflammation highlight a complex network where modulation of autophagy could potentially offer therapeutic benefits against cancer development and inflammatory diseases. Understanding these connections is crucial for developing targeted treatments that can selectively enhance or inhibit autophagy to manage these conditions effectively.
The central challenge in understanding the interplay between autophagy, solid tumors, and inflammation lies in deciphering how autophagy's dual role can be manipulated to suppress cancer growth while simultaneously controlling inflammatory responses. Autophagy can help eliminate oncogenic stimuli and damaged cells to prevent cancer onset; however, once cancer is established, it may contribute to tumor survival. Moreover, autophagy's role in managing inflammation—by controlling immune cell function and cytokine production—adds yet another layer of complexity, as both excessive or insufficient inflammation can promote tumorigenesis.
Addressing this problem requires a multi-faceted approach. Firstly, developing precise biomarkers that can accurately measure autophagic activity in specific contexts is essential. This will enable the identification of stages at which autophagy promotes either tumorigenesis or tumor suppression. Secondly, designing drugs that can modulate autophagy with high specificity will be crucial. These drugs need to selectively enhance autophagy to remove damaged cells and suppress inflammation without supporting cancer cell survival. Integrating these strategies into clinical trials will help validate the therapeutic potential of autophagy modulation in solid tumors and inflammatory diseases, paving the way for new treatment paradigms.
This Research Topic seeks to explore the intricate relationships between autophagy, solid tumors, and inflammation, aiming to unravel the complex mechanisms by which autophagy influences cancer progression and the inflammatory response. We invite authors to contribute original research papers, comprehensive reviews, and insightful clinical studies that delve into specific themes within this scope. Key themes of interest include the role of autophagy in solid tumor initiation and progression, the mechanisms by which autophagy regulates inflammatory pathways, and the impact of autophagy on the tumor microenvironment of solid tumors. Additionally, studies that investigate the therapeutic potential of modulating autophagy in cancer and inflammatory diseases are highly encouraged. By gathering diverse contributions from these areas, this research topic aims to build a deeper understanding of how autophagy can be targeted to develop innovative therapeutic strategies in the context of solid tumors and inflammation.
Please note: Manuscripts consisting solely of bioinformatics, computational analysis, or predictions of public databases which are not accompanied by validation (independent clinical or patient cohort, or biological validation in vitro or in vivo, which are not based on public databases) are not suitable for publication in this journal.