Deubiquitinase USP35 modulates ferroptosis in lung cancer via targeting ferroportin

Tang, Zheng; Jiang, Wanli; Mao, Ming; Zhao, Jinping; Chen, Jiakuan; Cheng, Nitao

doi:10.1002/ctm2.390

Cited by 100 publications

(86 citation statements)

References 66 publications

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“…verified that USP35 could maintain the stability of its protein by deubiquitinating FPN1, and reduce the iron disorder triggered by erastin/RSL3, thereby promoting lung cancer cell growth and tumor progression. Meanwhile, knockdown of USP35 enhanced the sensitivity of lung cancer cells to cisplatin and paclitaxel by targeting FPN1 in lung cancer ( 94 ). However, a study showed that matrix/macrophage expression of Lcn-2 was associated with tumor onset, lung metastasis, and recurrence, whereas FPN1 was not by analyzing the expression profiles of lipocalin-2 ( Lcn-2 ) and FPN1 through a model of T-oncogene (PyMT) breast cancer in spontaneous polymerases and mining publicly available TCGA and GEO database from gene expression synthesis ( 95 ).…”

Section: Iron Metabolism In Cancermentioning

confidence: 99%

The Role of Iron in Cancer Progression

et al. 2021

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Iron is an essential trace element for the human body, and its deficiency or excess can induce a variety of biological processes. Plenty of evidences have shown that iron metabolism is closely related to the occurrence and development of tumors. In addition, iron plays an important role in cell death, which is very important for the development of potential strategies for tumor treatment. Here, we reviewed the latest research about iron metabolism disorders in various types of tumors, the functions and properties of iron in ferroptosis and ferritinophagy, and new opportunities for iron-based on treatment methods for tumors, providing more information regarding the prevention and treatment of tumors.

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Section: Iron Metabolism In Cancermentioning

confidence: 99%

The Role of Iron in Cancer Progression

et al. 2021

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“…Several studies revealed that iron is closely associated with the development of lung cancer, and the disruption of iron homeostasis makes cells more sensitive to ferroptosis ( Kuang and Wang, 2019 ). USP35 is abundant in lung cancer cells and acts as a deubiquitinase to maintain the protein stability of ferroportin, which is a cellular efflux channel for iron ( Tang et al, 2021 ). Depletion of USP35 can promote ferroptotic cell death and sensitivity to cisplatin and paclitaxel chemotherapy in lung cancer cells ( Tang et al, 2021 ).…”

Section: Role Of Ferroptosis In Cancersmentioning

confidence: 99%

“…USP35 is abundant in lung cancer cells and acts as a deubiquitinase to maintain the protein stability of ferroportin, which is a cellular efflux channel for iron ( Tang et al, 2021 ). Depletion of USP35 can promote ferroptotic cell death and sensitivity to cisplatin and paclitaxel chemotherapy in lung cancer cells ( Tang et al, 2021 ). The iron-sulfur cluster biosynthetic enzyme NFS1 is overexpressed in well-differentiated lung adenocarcinomas and protects cells from ferroptosis within high oxygen environment by sustaining the levels of iron-sulfur cofactors ( Alvarez et al, 2017 ).…”

Section: Role Of Ferroptosis In Cancersmentioning

confidence: 99%

Ferroptosis-mediated Crosstalk in the Tumor Microenvironment Implicated in Cancer Progression and Therapy

Liu

Duan

Dai

et al. 2021

Front. Cell Dev. Biol.

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Ferroptosis is a recently recognized form of non-apoptotic regulated cell death and usually driven by iron-dependent lipid peroxidation and has arisen to play a significant role in cancer biology. Distinct from other types of cell death in morphology, genetics, and biochemistry, ferroptosis is characterized by the accumulation of lipid peroxides and lethal reactive oxygen species controlled by integrated oxidant and antioxidant systems. Increasing evidence indicates that a variety of biological processes, including amino acid, iron, lactate, and lipid metabolism, as well as glutathione, phospholipids, NADPH, and coenzyme Q10 biosynthesis, are closely related to ferroptosis sensitivity. Abnormal ferroptotic response may modulate cancer progression by reprogramming the tumor microenvironment (TME). The TME is widely associated with tumor occurrence because it is the carrier of tumor cells, which interacts with surrounding cells through the circulatory and the lymphatic system, thus influencing the development and progression of cancer. Furthermore, the metabolism processes play roles in maintaining the homeostasis and evolution of the TME. Here, this review focuses on the ferroptosis-mediated crosstalk in the TME, as well as discussing the novel therapeutic strategies for cancer treatment.

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“…Ubiquitin‐specific protease 35 (USP35) is a deubiquitinase that is overexpressed in lung cancer, and its knockdown, in addition to promoting ferroptosis and chemotherapeutic sensitivity to cisplatin and paclitaxel, inhibits lung cancer cell growth, colony formation, and tumor progression. The mechanism by which USP35 overexpression led to ferroptosis was attributed to ferroportin (FPN) stabilization, a protein responsible for exporting iron to the outside of the cells ( Figure 3 ) ( 55 ). In the same way, a similar relationship between deubiquitinase USP11 and NRF2 was found in patients with NSCLC (SCC subtype), leading to ferroptosis resistance and cell proliferation ( Figure 3 ) ( 56 ).…”

Section: Ferroptosis Regulators In Lung Cancermentioning

confidence: 99%

Ferroptosis in Lung Cancer: From Molecular Mechanisms to Prognostic and Therapeutic Opportunities

2021

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Lung cancer is the second commonly diagnosed malignancy worldwide and has the highest mortality rate among all cancers. Tremendous efforts have been made to develop novel strategies against lung cancer; however, the overall survival of patients still is low. Uncovering underlying molecular mechanisms of this disease can open up new horizons for its treatment. Ferroptosis is a newly discovered type of programmed cell death that, in an iron-dependent manner, peroxidizes unsaturated phospholipids and results in the accumulation of radical oxygen species. Subsequent oxidative damage caused by ferroptosis contributes to cell death in tumor cells. Therefore, understanding its molecular mechanisms in lung cancer appears as a promising strategy to induce ferroptosis selectively. According to evidence published up to now, significant numbers of research have been done to identify ferroptosis regulators in lung cancer. Therefore, this review aims to provide a comprehensive standpoint of molecular mechanisms of ferroptosis in lung cancer and address these molecules’ prognostic and therapeutic values, hoping that the road for future studies in this field will be paved more efficiently.

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Deubiquitinase USP35 modulates ferroptosis in lung cancer via targeting ferroportin

Abstract: 1. USP35 is abundant in human lung cancer tissues and cell lines. 2. USP35 modulates iron homeostasis and ferroptosis in lung cancer tissues and cell lines.3. USP35 directly interacts with ferroportin and maintain its protein stability to prevent iron overload and ferroptosis.

Cited by 100 publications

References 66 publications

The Role of Iron in Cancer Progression

The Role of Iron in Cancer Progression

Ferroptosis-mediated Crosstalk in the Tumor Microenvironment Implicated in Cancer Progression and Therapy

Ferroptosis in Lung Cancer: From Molecular Mechanisms to Prognostic and Therapeutic Opportunities

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