Mitochondria in Cancer Stem Cells: Implication in Molecular Diagnosis and Therapeutics

About this Research Topic

Submission deadlines

  1. Manuscript Summary Submission Deadline 15 June 2025 | Manuscript Submission Deadline 30 September 2025

  2. This Research Topic is still accepting articles.

Background

The exploration of mitochondrial mechanisms in cancer stem cells (CSCs) presents a promising frontier in cancer research, with significant implications for molecular diagnosis and therapeutic strategies. This collection invites contributions from diverse fields to deepen our understanding of how mitochondrial functions influence the metabolic characteristics of CSCs and their role in cancer progression.

Cancer is increasingly recognized as a stem cell disease, with CSCs exhibiting unique metabolic profiles that differentiate them from differentiated tumor cells. While traditional views emphasized glycolysis as the primary energy source for cancer cells, emerging evidence suggests that mitochondrial metabolism plays a crucial role in the survival and functionality of CSCs. This duality in energy production—where CSCs can switch between glycolysis and oxidative phosphorylation (OXPHOS)—enables them to adapt to varying micro-environmental conditions, contributing to their resilience against conventional therapies and their potential for tumor relapse.

Cancer stem cells (CSCs) exhibit extensive metabolic flexibility, thriving in hypoxic tumor environments through dynamic mitochondrial shifts that manage energy production based on nutrient availability and oxygen levels. This metabolic plasticity is crucial for their survival, making mitochondria central to CSC drug resistance mechanisms and vital targets for new therapies. Research into mitochondrial dynamics can enhance treatment efficacy by revealing drug resistance pathways and metabolic vulnerabilities. Additionally, identifying unique metabolic phenotypes of CSCs can advance molecular diagnostics, enabling early detection, accurate prognosis, and more personalized treatment strategies, all while potentially sparing normal cells.


We invite researchers and practitioners from various disciplines—including molecular biology, oncology, pharmacology, and clinical research—to submit original articles, reviews, and case studies that explore the implications of mitochondrial metabolism in cancer stem cells.



Contributions may focus but not restricted to the followings:

· Mitochondrial DNA mutations as biomarkers for CSC identification and prognosis

· Mitochondrial metabolites as biomarkers for CSC identification and prognosis · Mechanistic insights into mitochondrial roles in CSC metabolism.

· Role of mitochondria in cancer stem cell quiescence

· Mitochondrial dynamics in CSC plasticity and therapy resistance

· Role of autophagy and mitophagy in CSCs and their potential as therapeutic targeting

· Metabolic flexibility in CSCs: Switching between Glycolysis and OXPHOS

· Mitochondrial biogenesis and its role in drug resistance in CSCs

· Interplay between mitochondrial metabolism and epigenetic regulation in CSCs

· Mitochondrial ROS: Crucial Drivers of CSC Survival and Metastasis

· Role of tumor microenvironment and mitochondrial metabolism in CSCs

· Advanced technologies for the detection of mitochondrial metabolomics in CSCs

· Therapeutic Targeting of Mitochondrial Function in CSCs: Preclinical and clinical studies

This collection aims to foster interdisciplinary dialogue and collaboration, ultimately enhancing our understanding of CSC metabolism and its potential for transforming cancer diagnosis and treatment. Submissions are welcomed that advance the field and contribute to the ongoing discourse on this critical topic.

Article types and fees

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

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  • Editorial
  • General Commentary
  • Hypothesis and Theory
  • Methods
  • Mini Review
  • Opinion
  • Original Research
  • Perspective

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Keywords: cancer stem cells, csc, molecular diagnosis, Mitochondrial DNA

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