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Review
. 2024 Nov 23;17(1):233.
doi: 10.1186/s13048-024-01560-8.

Unveiling the power of mitochondrial transfer in cancer progression: a perspective in ovarian cancer

Caixia Wang  1   2 , Chuan Xie  3   4
Affiliations
Review

Unveiling the power of mitochondrial transfer in cancer progression: a perspective in ovarian cancer

Caixia Wang et al. J Ovarian Res. .

Abstract

Mitochondria are dynamic organelles integral to metabolic processes, coordination of essential biological pathways, and oncogenesis and tumor progression. Recent studies have revealed that mitochondria can be transferred between cells via multiple mechanisms, implicating their involvement in the pathogenesis and progression of ovarian cancer. This review provides a comprehensive analysis of intercellular mitochondrial transfer within the context of ovarian cancer and its tumor microenvironment. We also propose targeted pathways and therapeutic strategies that could be utilized to modulate diseases associated with mitochondrial transfer therapy. Finally, we examine recent advancements in this field and identify several unresolved questions.

Keywords: Mitochondrial transfer; Ovarian Cancer; Targeted therapy; Tumor Microenvironment.

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Conflict of interest statement

Declarations. Ethics approval and consent to participate: Not applicable. Consent for publication: All authors gave their consent for publication. Competing interests: The authors declare no competing interests.

Figures

Fig. 1
Fig. 1
TNTs-mediated intercellular mitochondrial transfer and signaling pathways. The mTOR/Cdc42 and EGFR/MEK signaling pathways are implicated in the formation of TNTs. Miro1 is primarily accountable for transporting mitochondria
Fig. 2
Fig. 2
Mitochondrial transfer via EVs and the molecular pathways implicated. CD38 catalyzes the NAD+ to cADPR, and increases the release of Ca2+ from endoplasmic reticulum, thus promoting the release of mitochondria-containing MVs. ARRDC1 interact with TSG101 and unload mitochondria outward the plasma membrane
Fig. 3
Fig. 3
Cell fusion-mediated intercellular mitochondrial transfer and signaling pathways. VCAM-1/VLA-4, syncytin-1/ASCT-2, and syncytin-2/ MFSD-2 mediate the process of cell fusion. TNFα can increase the expression of syncytin-1 and ASCT-2 via PI3K/AKT and Wnt/β-catenin signaling pathways respectively
Fig. 4
Fig. 4
Uptake of isolated mitochondria and implicated signaling pathways. Ras activates the subsequent cascades such as PI3K, Rab5, Arf6, and Rac1/Cdc42/PAK1, thereby mediating macropinocytic activity
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