Autophagy-dependent ferroptosis drives tumor-associated macrophage polarization via release and uptake of oncogenic KRAS protein

Dai, Enyong; Han, Leng; Liu, Jiao; Xie, Yangchun; Kroemer, Guido; Klionsky, Daniel J.; Zeh, Herbert J.; Kang, Rui; Wang, Jing; Tang, Daolin

doi:10.1080/15548627.2020.1714209

Cited by 416 publications

(315 citation statements)

References 88 publications

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“…For example, ferroptotic cancer cells release oncogenic KRAS protein which can be engulfed and drive tumor-associated macrophage polarization. 112 Ferroptosis also occurs in macrophages. [113][114][115] However, compared with cancer cells, macrophages exert higher resistance to ferroptosis.…”

Section: The Interaction Of Ferroptosis and Lipid Metabolism Modulatementioning

confidence: 99%

The interaction between ferroptosis and lipid metabolism in cancer

2020

Sig Transduct Target Ther

426

285

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Ferroptosis is a new form of programmed cell death characterized by the accumulation of iron-dependent lethal lipid peroxides. Recent discoveries have focused on alterations that occur in lipid metabolism during ferroptosis and have provided intriguing insights into the interplay between ferroptosis and lipid metabolism in cancer. Their interaction regulates the initiation, development, metastasis, therapy resistance of cancer, as well as the tumor immunity, which offers several potential strategies for cancer treatment. This review is a brief overview of the features characterizing the interaction between ferroptosis and lipid metabolism, and highlights the significance of this interaction in cancer.

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Section: The Interaction Of Ferroptosis and Lipid Metabolism Modulatementioning

confidence: 99%

The interaction between ferroptosis and lipid metabolism in cancer

2020

Sig Transduct Target Ther

426

285

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“…Two major subtypes of tumor-associated macrophages (TAMs) are generated depending on different environmental stresses, including antitumor M1 and procarcinogenic M2 TAMs (111). The KRAS G12D protein released from ferroptotic pancreatic cancer cells is further absorbed by macrophages through an advanced glycosylation end product-specific receptor, which then induces STAT3-dependent fatty acid oxidation and drives macrophages to form M2-like TAMs (112). Oxidized phosphatidylcholine from ferroptotic cancer cells also inhibits DC maturation and inhibits the differentiation of T helper 17 (TH17) cells through activation of NRF2 (113).…”

Section: Ferroptosis In Tumor Microenvironments and Immunotherapy Ofmentioning

confidence: 99%

Ferroptosis in Cancer Treatment: Another Way to Rome

Luo

et al. 2020

Front. Oncol.

124

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Ferroptosis is a newly described type of programmed cell death and intensively related to both maintaining homeostasis and the development of diseases, especially cancers. Inducing ferroptosis leads to mitochondrial dysfunction and toxic lipid peroxidation in cells, which plays a pivotal role in suppressing cancer growth and progression. Here, we reviewed the existing studies about the molecular mechanisms of ferroptosis involved in different antitumor treatments, such as chemotherapy, targeted therapy, radiotherapy, and immunotherapy. We focused in particular on the distinct combinatorial therapeutic effects such as the synergistic sensitization effect and the drug-resistance reversal achieved when using ferroptosis inducers with conventional cancer therapy. Finally, we discussed the challenges and opportunities in clinical applications of ferroptosis. The application of nanotechnolgy and other novel technologies may provide a new direction in ferroptosis-driven cancer therapies.

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“…Biochemically, ferroptosis can be suppressed by various small molecules, involving iron chelators (e.g., deferoxamine), lipophilic antioxidants (e.g., α -tocopherol), and lipid peroxidation inhibitors [ 21 – 24 ] that to the maximum extent do not similar with other forms of RCD [ 1 , 5 , 25 , 26 ]. Moreover, while numerous genes including p53 [ 7 , 27 , 28 ], nuclear factor E2-related factor 2 ( Nrf2 ) [ 29 , 30 ], and autophagy-related ( ATG ) genes [ 9 , 31 ] modulate different RCDs, a distinct set of genes such as ribosomal protein L8 ( RPL8 ), ATP synthase F0 complex subunit C3 ( ATP5G3 ), tetratricopeptide repeat domain 35 ( TTC35 ), citrate synthase, and iron response element binding protein 2 ( IREB2 ) seems peculiar to regulate ferroptosis [ 1 ]. As ferroptosis shares different mechanisms with other forms of cell death, it could unquestionably circumvent their limitations.…”

Section: Main Textmentioning

confidence: 99%

Molecular Mechanisms of Ferroptosis and Its Role in Pulmonary Disease

Tao

Liu

2020

Oxidative Medicine and Cellular Longevity

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Ferroptosis is a new mode of cell death that is characterized by the excessive accumulation of iron and lipid peroxides. It has unique morphological changes and disparate biochemical features and plays an intricate role in many pathophysiological processes. A great deal of researches confirms that ferroptosis can be regulated by numerous molecules through different mechanisms, supporting great potentials for novel pharmacological therapeutics. Recently, several studies reveal that ferroptosis is also closely associated with the initiation and development of respiratory disease. Understanding the specific mechanism, the molecular trait of ferroptosis and their relationship with pulmonary disease could provide significant references regarding effective treatment of these obstinate disease.

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Autophagy-dependent ferroptosis drives tumor-associated macrophage polarization via release and uptake of oncogenic KRAS protein

Cited by 416 publications

References 88 publications

The interaction between ferroptosis and lipid metabolism in cancer

The interaction between ferroptosis and lipid metabolism in cancer

Ferroptosis in Cancer Treatment: Another Way to Rome

Molecular Mechanisms of Ferroptosis and Its Role in Pulmonary Disease

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