Boosting the Ferroptotic Antitumor Efficacy via Site-Specific Amplification of Tailored Lipid Peroxidation

An, Yang; Zhu, Jingjing; Liu, Fang; Deng, Jian Hong; Meng, Xuan; Liu, Guangqin; Wu, Hsiao-Ming; Fan, Aiping; Wang, Zheng; Zhao, Yanjun

doi:10.1021/acsami.9b10954

Cited by 79 publications

(69 citation statements)

References 60 publications

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“…Recently, nanocarriers have been proposed as an efficient approach to induce ferroptosis in cancer cells in vitro and in vivo [121]. Doxorubicin, packed into mesoporous carbon nanoparticles, induces ferroptosis in breast cancer (MCF7) cells, in A549 cells, and in human cervical carcinoma (HeLa) cells [122].…”

Section: Ferroptosis Is a New Promising Target For Cancer Treatmentmentioning

confidence: 99%

Ferroptosis and Cancer: Mitochondria Meet the “Iron Maiden” Cell Death

Battaglia

Chirillo

Aversa

et al. 2020

Cells

357

232

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Ferroptosis is a new type of oxidative regulated cell death (RCD) driven by iron-dependent lipid peroxidation. As major sites of iron utilization and master regulators of oxidative metabolism, mitochondria are the main source of reactive oxygen species (ROS) and, thus, play a role in this type of RCD. Ferroptosis is, indeed, associated with severe damage in mitochondrial morphology, bioenergetics, and metabolism. Furthermore, dysregulation of mitochondrial metabolism is considered a biochemical feature of neurodegenerative diseases linked to ferroptosis. Whether mitochondrial dysfunction can, per se, initiate ferroptosis and whether mitochondrial function in ferroptosis is context-dependent are still under debate. Cancer cells accumulate high levels of iron and ROS to promote their metabolic activity and growth. Of note, cancer cell metabolic rewiring is often associated with acquired sensitivity to ferroptosis. This strongly suggests that ferroptosis may act as an adaptive response to metabolic imbalance and, thus, may constitute a new promising way to eradicate malignant cells. Here, we review the current literature on the role of mitochondria in ferroptosis, and we discuss opportunities to potentially use mitochondria-mediated ferroptosis as a new strategy for cancer therapy.

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Section: Ferroptosis Is a New Promising Target For Cancer Treatmentmentioning

confidence: 99%

Ferroptosis and Cancer: Mitochondria Meet the “Iron Maiden” Cell Death

Battaglia

Chirillo

Aversa

et al. 2020

Cells

357

232

View full text Add to dashboard Cite

show abstract

“…An et al combined nanocarriers loading Fe 3+ and RSL3 with ascorbate (Asc), which was reported to selectively kill cancer cells by accumulating hydrogen peroxide (H 2 O 2 ) only in tumour extracellular fluids, to induce ferroptosis in cancer cells more accurately [111].…”

Section: Development Of Ferroptotic Therapeutic Strategiesmentioning

confidence: 99%

Targeting ferroptosis in breast cancer

et al. 2020

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Ferroptosis is a recently discovered distinct type of regulated cell death caused by the accumulation of lipid-based ROS. Metabolism and expression of specific genes affect the occurrence of ferroptosis, making it a promising therapeutic target to manage cancer. Here, we describe the current status of ferroptosis studies in breast cancer and trace the key regulators of ferroptosis back to previous studies. We also compare ferroptosis to common regulated cell death patterns and discuss the sensitivity to ferroptosis in different subtypes of breast cancer. We propose that viewing ferroptosis-related studies from a historical angle will accelerate the development of ferroptosis-based biomarkers and therapeutic strategies in breast cancer.

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“…DOPA has been widely employed for engineering inorganic-organic hybrid drug delivery particles. [40,41] DSPE-PEG was deposited onto CA4P or DOPA layer through hydrophobic interaction to stabilize nanocarriers via steric mechanism.…”

Section: Resultsmentioning

confidence: 99%

Double‐Lock Nanomedicines Enable Tumor‐Microenvironment‐Responsive Selective Antitumor Therapy

Liu

Zhu

Dai

et al. 2021

Adv Funct Materials

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A hybrid nanocarrier for reducing the off-target adverse effects of chemotherapy via selective drug delivery to the tumor cells is reported. The model active agent, combretastatin A4 (CA4) phosphate is deposited onto the magnetite (Fe 3 O 4 ) nanoparticles as the core, followed by lipid coating as the shell. Upon nanocarrier administration and biodistribution to the tumor site, the high level of adenosine triphosphate in the extracellular space of tumor induces the cargo release via phosphate displacement. Then, the CA4 phosphate is dephosphorylated by the alkaline phosphatase that is overexpressed at the plasma membrane of certain tumor cells, resulting in enhanced intracellular uptake of hydrophobic CA4. These sequential two-step unlocking processes enable the preferable accumulation of CA4 within tumor cells. Such approach is applicable to a wide range of chemotherapeutics and is promising for efficacy enhancement and side-effect reduction of antitumor chemotherapy.

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Boosting the Ferroptotic Antitumor Efficacy via Site-Specific Amplification of Tailored Lipid Peroxidation

Cited by 79 publications

References 60 publications

Ferroptosis and Cancer: Mitochondria Meet the “Iron Maiden” Cell Death

Ferroptosis and Cancer: Mitochondria Meet the “Iron Maiden” Cell Death

Targeting ferroptosis in breast cancer

Double‐Lock Nanomedicines Enable Tumor‐Microenvironment‐Responsive Selective Antitumor Therapy

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