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Review
. 2021 Mar 18:11:629614.
doi: 10.3389/fonc.2021.629614. eCollection 2021.

Potential Mechanism Underlying the Role of Mitochondria in Breast Cancer Drug Resistance and Its Related Treatment Prospects

Affiliations
Review

Potential Mechanism Underlying the Role of Mitochondria in Breast Cancer Drug Resistance and Its Related Treatment Prospects

Yuefeng Li et al. Front Oncol. .

Abstract

Breast cancer incidence and mortality rates have been consistently high among women. The use of diverse therapeutic strategies, including chemotherapy, endocrine therapy, targeted therapy, and immunotherapy, has improved breast cancer prognosis. However, drug resistance has become a tremendous obstacle in overcoming breast cancer recurrence and metastasis. It is known that mitochondria play an important role in carcinoma cell growth, invasion and apoptosis. Recent studies have explored the involvement of mitochondrial metabolism in breast cancer prognosis. Here, we will provide an overview of studies that investigated mitochondrial metabolism pathways in breast cancer treatment resistance, and discuss the application prospects of agents targeting mitochondrial pathways against drug-resistant breast cancer.

Keywords: breast cancer; chemoresistance; drug resistance; mitochondrial; tumor microenvironment.

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Conflict of interest statement

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Figures

Figure 1
Figure 1
A diagram of the relationship between key molecules in the microenvironment of drug-resistant breast cancer tumors and mitochondria, and the mechanism of the relevant drugs. CAV‐1, caveolin‐1; MCT4, monocarboxylate transporter 4; ROS, reactive oxygen species; SOD2, superoxide dismutase 2; AS‐IV, astragaloside IV; NO, nitric oxide.
Figure 2
Figure 2
A diagram of some mechanism of mitochondria involved in apoptosis-mediated breast cancer drug resistance and related drugs. BH3, BCL-2 homology domain 3.

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