Cancer stem cells: mitochondria signalling pathway and strategies for therapeutic interventions.
- Publisher:
- Springer Nature
- Publication Type:
- Journal Article
- Citation:
- Mol Biol Rep, 2025, 52, (1), pp. 671
- Issue Date:
- 2025-07-03
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Full metadata record
| Field | Value | Language |
|---|---|---|
| dc.contributor.author | Tan, EW | |
| dc.contributor.author | Singh, SK | |
| dc.contributor.author |
Dua, K |
|
| dc.contributor.author | Gupta, G | |
| dc.contributor.author | Lee, WL | |
| dc.contributor.author | Wong, RSY | |
| dc.contributor.author | Tan, KO | |
| dc.contributor.author | Goh, BH | |
| dc.date.accessioned | 2025-07-19T07:09:01Z | |
| dc.date.available | 2025-06-18 | |
| dc.date.available | 2025-07-19T07:09:01Z | |
| dc.date.issued | 2025-07-03 | |
| dc.identifier.citation | Mol Biol Rep, 2025, 52, (1), pp. 671 | |
| dc.identifier.issn | 0301-4851 | |
| dc.identifier.issn | 1573-4978 | |
| dc.identifier.uri | http://hdl.handle.net/10453/188556 | |
| dc.description.abstract | Cancer stem cells (CSCs) play a critical role in tumor initiation, progression, and resistance to therapy, making them a major hurdle in effective cancer treatment. Unlike bulk cancer cells, CSCs exhibit remarkable adaptability, allowing them to survive under metabolic stress and evade conventional therapies. Mitochondria, as central regulators of cellular metabolism and apoptosis, are integral to CSC function. They facilitate metabolic reprogramming, redox balance, and stress adaptation, thereby enhancing CSC survival, self-renewal, and resistance to treatment. Dysregulated mitochondrial dynamics, including alterations in biogenesis, degradation, and signaling pathways, contribute to CSC maintenance and therapeutic resistance. Furthermore, mitochondrial membrane integrity and oxidative stress regulation determine CSC fate, influencing their ability to withstand chemotherapy and radiotherapy. Recent advances have identified mitochondrial-targeted strategies as promising approaches to impair CSC function and sensitize them to treatment. These include disrupting mitochondrial metabolism, inducing oxidative stress, and modulating mitochondrial quality control mechanisms. By understanding the intricate relationship between mitochondria and CSCs, new therapeutic strategies can be developed to selectively target CSCs, ultimately improving cancer treatment outcomes and preventing disease recurrence. This review provides an in-depth analysis of mitochondrial mechanisms in CSCs and their potential as therapeutic targets. | |
| dc.format | Electronic | |
| dc.language | eng | |
| dc.publisher | Springer Nature | |
| dc.relation.ispartof | Mol Biol Rep | |
| dc.relation.isbasedon | 10.1007/s11033-025-10748-0 | |
| dc.rights | info:eu-repo/semantics/openAccess | |
| dc.subject | 0601 Biochemistry and Cell Biology | |
| dc.subject.classification | Biochemistry & Molecular Biology | |
| dc.subject.classification | 3101 Biochemistry and cell biology | |
| dc.subject.mesh | Humans | |
| dc.subject.mesh | Neoplastic Stem Cells | |
| dc.subject.mesh | Mitochondria | |
| dc.subject.mesh | Signal Transduction | |
| dc.subject.mesh | Oxidative Stress | |
| dc.subject.mesh | Neoplasms | |
| dc.subject.mesh | Animals | |
| dc.subject.mesh | Mitochondrial Dynamics | |
| dc.subject.mesh | Apoptosis | |
| dc.subject.mesh | Mitochondria | |
| dc.subject.mesh | Animals | |
| dc.subject.mesh | Humans | |
| dc.subject.mesh | Neoplasms | |
| dc.subject.mesh | Signal Transduction | |
| dc.subject.mesh | Apoptosis | |
| dc.subject.mesh | Oxidative Stress | |
| dc.subject.mesh | Neoplastic Stem Cells | |
| dc.subject.mesh | Mitochondrial Dynamics | |
| dc.subject.mesh | Humans | |
| dc.subject.mesh | Neoplastic Stem Cells | |
| dc.subject.mesh | Mitochondria | |
| dc.subject.mesh | Signal Transduction | |
| dc.subject.mesh | Oxidative Stress | |
| dc.subject.mesh | Neoplasms | |
| dc.subject.mesh | Animals | |
| dc.subject.mesh | Mitochondrial Dynamics | |
| dc.subject.mesh | Apoptosis | |
| dc.title | Cancer stem cells: mitochondria signalling pathway and strategies for therapeutic interventions. | |
| dc.type | Journal Article | |
| utslib.citation.volume | 52 | |
| utslib.location.activity | Netherlands | |
| utslib.for | 0601 Biochemistry and Cell Biology | |
| pubs.organisational-group | University of Technology Sydney | |
| pubs.organisational-group | University of Technology Sydney/Faculty of Health | |
| pubs.organisational-group | University of Technology Sydney/UTS Groups | |
| pubs.organisational-group | University of Technology Sydney/UTS Groups/Centre for Inflammation (CFI) | |
| pubs.organisational-group | University of Technology Sydney/UTS Groups/Centre for Inflammation (CFI)/Centre for Inflammation (CFI) Associate Members | |
| pubs.organisational-group | University of Technology Sydney/UTS Groups/Australian Research Consortium in Complementary and Integrative Medicine (ARCCIM) | |
| pubs.organisational-group | University of Technology Sydney/UTS Groups/Stroke Research Collaborative | |
| utslib.copyright.status | open_access | * |
| dc.rights.license | This work is licensed under a Creative Commons Attribution 4.0 International License (CC BY 4.0). To view a copy of this license, visit https://creativecommons.org/licenses/by/4.0/ | |
| dc.date.updated | 2025-07-19T07:08:59Z | |
| pubs.issue | 1 | |
| pubs.publication-status | Published online | |
| pubs.volume | 52 | |
| utslib.citation.issue | 1 |
Abstract:
Cancer stem cells (CSCs) play a critical role in tumor initiation, progression, and resistance to therapy, making them a major hurdle in effective cancer treatment. Unlike bulk cancer cells, CSCs exhibit remarkable adaptability, allowing them to survive under metabolic stress and evade conventional therapies. Mitochondria, as central regulators of cellular metabolism and apoptosis, are integral to CSC function. They facilitate metabolic reprogramming, redox balance, and stress adaptation, thereby enhancing CSC survival, self-renewal, and resistance to treatment. Dysregulated mitochondrial dynamics, including alterations in biogenesis, degradation, and signaling pathways, contribute to CSC maintenance and therapeutic resistance. Furthermore, mitochondrial membrane integrity and oxidative stress regulation determine CSC fate, influencing their ability to withstand chemotherapy and radiotherapy. Recent advances have identified mitochondrial-targeted strategies as promising approaches to impair CSC function and sensitize them to treatment. These include disrupting mitochondrial metabolism, inducing oxidative stress, and modulating mitochondrial quality control mechanisms. By understanding the intricate relationship between mitochondria and CSCs, new therapeutic strategies can be developed to selectively target CSCs, ultimately improving cancer treatment outcomes and preventing disease recurrence. This review provides an in-depth analysis of mitochondrial mechanisms in CSCs and their potential as therapeutic targets.
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