Metabolic and Cellular Stress Responses in Cancer Progression and Therapy Resistance

Proposed Abstract:

Cancer cells are exposed to constant metabolic and cellular stress as they adapt to rapid growth, limited nutrient availability, oxidative imbalance, hypoxia, endoplasmic reticulum stress, genomic instability, and therapeutic pressure. Rather than acting only as damaging conditions, these stress signals shape cancer cell behaviour by regulating survival, senescence, apoptosis, plasticity, proliferation, and resistance to treatment.



Metabolic reprogramming and stress-response pathways are now recognized as central drivers of cancer progression, therapeutic response, and disease evolution. Altered glucose metabolism, mitochondrial dysfunction, oxidative stress, unfolded protein response signaling, autophagy, senescence-associated programs, and immunometabolic adaptations can all influence tumor cell fate and therapeutic vulnerability. These mechanisms are particularly relevant in solid tumors, where stress-adaptive responses help cancer cells survive metabolically challenging microenvironments and evade conventional or targeted therapies.



This Research Topic aims to bring together mechanistic, translational, and multi-omics studies that explore how metabolic and cellular stress responses contribute to cancer progression, metastasis dissemination, therapeutic response, and resistance. We welcome studies that identify stress-regulated pathways, biomarkers, and therapeutic targets to advance our understanding of tumor biology and support the development of more effective treatment strategies.



Proposed Scope: This Research Topic will focus on the role of metabolic and cellular stress responses in cancer cell behavior, tumor progression, and therapeutic resistance. We welcome original research, reviews, mini reviews, perspectives, and other article types accepted by Frontiers.



Areas of interest include, but are not limited to:



- Metabolic stress and cancer cell fate decisions, including survival, apoptosis, senescence, and plasticity

- Endoplasmic reticulum stress, unfolded protein response signaling, and PERK-related pathways in cancer progression

- Oxidative stress, reactive oxygen species, and redox regulation in tumor biology

- Mitochondrial dysfunction and metabolic reprogramming in solid tumors

- Autophagy and stress-adaptive mechanisms in cancer cell survival

- Senescence-associated programs and their role in tumor progression or therapy response

- Immunometabolic adaptations and tumor-immune microenvironment crosstalk under metabolic stress

- Multi-omics approaches (genomics, transcriptomics, proteomics, metabolomics) to characterizing stress adaptation and disease evolution in tumors

- Stress-response pathways involved in chemotherapy, targeted therapy, radiotherapy, or immunotherapy resistance

- Mechanisms linking metabolic and cellular stress to tumor metastasis and dissemination

- Biomarkers of metabolic or cellular stress with diagnostic, prognostic, or therapeutic relevance

- Natural compounds or bioactive molecules targeting cancer cell stress pathways

- Mechanistic and translational studies using cancer cell models, organoids, patient-derived samples, animal models, or clinically relevant systems



Studies that are purely descriptive or based only on bioinformatic analysis without experimental validation or mechanistic insight may fall outside the scope of this collection.

Article types and fees

This Research Topic accepts the following article types, unless otherwise specified in the Research Topic description:

• Brief Research Report
• Data Report
• Editorial
• FAIR² Data
• General Commentary
• Hypothesis and Theory
• Methods
• Mini Review
• Opinion
• ... View all formats

Articles that are accepted for publication by our external editors following rigorous peer review incur a publishing fee charged to Authors, institutions, or funders.

Article types

This Research Topic accepts the following article types, unless otherwise specified in the Research Topic description:

• Brief Research Report
• Data Report
• Editorial
• FAIR² Data
• General Commentary
• Hypothesis and Theory
• Methods
• Mini Review
• Opinion
• Original Research
• Perspective
• Review
• Technology and Code

Keywords: Cancer cell metabolism, Cellular stress response, Metabolic reprogramming, Therapy resistance, Cancer cell fate

Important note: All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.