Adipose Stem Cells and Their Interplay with Cancer Cells and Mitochondrial Reservoir: A New Promising Target
by
, , , and
Ayesha Rehman
1
,
Martina Marigliano
2,
Martina Torsiello
1,
Marcella La Noce
1
,
Gianpaolo Papaccio
1,*
,
Virginia Tirino
1,
Vitale Del Vecchio
1 and
Federica Papaccio
2,*
1
Department of Experimental Medicine, Section of Human Histology and Embryology, University of Campania “L. Vanvitelli”, Via L. Armanni 5, 80128 Naples, NA, Italy
2
Department of Medicine, Surgery and Dentistry “Scuola Medica Salernitana”, Via S. Allende 43, 84081 Baronissi, SA, Italy
*
Authors to whom correspondence should be addressed.
Cancers 2024, 16(15), 2769; https://doi.org/10.3390/cancers16152769
Submission received: 11 July 2024
/
Revised: 31 July 2024
/
Accepted: 2 August 2024
/
Published: 5 August 2024
(This article belongs to the Section Cancer Therapy)
Simple Summary
Much interest has arisen around adipose-derived stem cells (ASCs) due to their multifunctional activities in the tumor microenvironment (TME). Mitochondrial dynamics and mitochondrial transfer are critical processes that promote tumor progression through fission, fusion, and transfer from stromal cells, such as ASCs. This perspective focuses on the connection between ASCs and tumor cells, leveraging the idea that inhibiting their possible pro-tumorigenic effect can interfere with these processes and limit the ability of tumor cells to survive. Unfortunately, the use of ASC/MSCs in cancer therapy has some limitations, as many variables must be considered; however, bridging the gap between preclinical studies and clinical applications could lead to new therapeutic strategies.
Abstract
Adipose-derived stem cells (ASCs) significantly influence tumor progression within the tumor microenvironment (TME). This review examines the pro-tumorigenic roles of ASCs, focusing on paracrine signaling, direct cell–cell interactions, and immunomodulation. ASC-mediated mitochondrial transfer through tunneling nanotubes (TNTs) and gap junctions (GJs) plays a significant role in enhancing cancer cell survival and metabolism. Cancer cells with dysfunctional mitochondria acquire mitochondria from ASCs to meet their metabolic needs and thrive in the TME. Targeting mitochondrial transfer, modulating ASC function, and influencing metabolic pathways are potential therapeutic strategies. However, challenges like TME complexity, specificity, safety concerns, and resistance mechanisms must be addressed. Disrupting the ASC–cancer cell–mitochondria axis offers a promising approach to cancer therapy.
Keywords:
ASCs; mitochondria; TME; CSCs; drug resistance; cancer therapy
