<i>RETRACTED:</i> Resibufogenin inhibited colorectal cancer cell growth and tumorigenesis through triggering ferroptosis and ROS production mediated by GPX4 inactivation

Shen, Liandong; Wen-hai, QI; Bai, Jiang-Jiang; Zuo, Chun-Yi; Bai, Donglin; Gao, Weidong; Xinling, Zong; Hao, Tingting; Ma, Yan; Guangcai, Cao

doi:10.1002/ar.24378

Cited by 53 publications

(39 citation statements)

References 31 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…It is capable of reducing the toxic, membranous lipid hydroperoxides into non-toxic lipid alcohols ( Brigelius-Flohé and Maiorino, 2013 ; Yang et al, 2014 ). Increasing GPX4 has been shown to be beneficial in many models of disease by inhibiting ferroptosis ( Lan et al, 2020 ; Shen et al, 2020 ). However, knockdown or inactivation of GPX4 contributes to the accumulation of lipid peroxidation and initiation of ferroptosis ( Park et al, 2019 ; Ye et al, 2020 ).…”

Section: Discovery and Mechanisms Of Ferroptosismentioning

confidence: 99%

Ferroptosis in Acute Central Nervous System Injuries: The Future Direction?

Shen

Lin

et al. 2020

Front. Cell Dev. Biol.

View full text Add to dashboard Cite

Acute central nervous system (CNS) injuries, such as stroke, traumatic brain injury (TBI), and spinal cord injury (SCI) present a grave health care challenge worldwide due to high morbidity and mortality, as well as limited clinical therapeutic strategies. Established literature has shown that oxidative stress (OS), inflammation, excitotoxicity, and apoptosis play important roles in the pathophysiological processes of acute CNS injuries. Recently, there have been many studies on the topic of ferroptosis, a form of regulated cell death characterized by the accumulation of iron-dependent lipid peroxidation. Some studies have revealed an emerging connection between acute CNS injuries and ferroptosis. Ferroptosis, induced by the abnormal metabolism of lipids, glutathione (GSH), and iron, can accelerate acute CNS injuries. However, pharmaceutical agents, such as iron chelators, ferrostatin-1 (Fer-1), and liproxstatin-1 (Lip-1), can inhibit ferroptosis and may have neuroprotective effects after acute CNS injuries. However, the specific mechanisms underlying this connection has not yet been clearly elucidated. In this paper, we discuss the general mechanisms of ferroptosis and its role in stroke, TBI, and SCI. We also summarize ferroptosis-related drugs and highlight the potential therapeutic strategies in treating various acute CNS injuries. Additionally, this paper suggests a testable hypothesis that ferroptosis may be a novel direction for further research of acute CNS injuries by providing corresponding evidence.

show abstract

Section: Discovery and Mechanisms Of Ferroptosismentioning

confidence: 99%

Ferroptosis in Acute Central Nervous System Injuries: The Future Direction?

Shen

Lin

et al. 2020

Front. Cell Dev. Biol.

View full text Add to dashboard Cite

show abstract

“…b-elemene and cetuximab, which were combined to treat KRAS mutant CRC cells, could induce ferroptosis (Chen et al, 2020). Shen et al demonstrated that RB could inactivate GPX4 to trigger ferroptosis in CRC cells, which can inhibit the growth of CRC cells and tumor formation (Shen et al, 2020).…”

Section: Colorectal Carcinomamentioning

confidence: 99%

“…Shen et al. demonstrated that RB could inactivate GPX4 to trigger ferroptosis in CRC cells, which can inhibit the growth of CRC cells and tumor formation ( Shen et al., 2020 ).…”

Section: The Link Between Ferroptosis and Cancermentioning

confidence: 99%

The Mechanism of Ferroptosis and Applications in Tumor Treatment

et al. 2020

View full text Add to dashboard Cite

Iron-dependent ferroptosis is a new form of cell death in recent years, which is driven by lipid peroxidation. The lethal lipid accumulation caused by glutathione depletion or inactivation of glutathione peroxidase 4 (GPX4) is characteristic of the ferroptosis process. In recent years, with the in-depth study of ferroptosis, various types of diseases have been reported to be related to ferroptosis. In other words, ferroptosis, which has attracted widespread attention in the fields of biochemistry, oncology, and especially materials science, can undoubtedly provide a new way for patients. This review introduces the relevant mechanisms of ferroptosis, the relationship between ferroptosis and various cancers, as well as the application of ferroptosis in tumor treatment. We also sorted out the genes and drugs that regulate ferroptosis. Moreover, small molecule compound-induced ferroptosis has a strong inhibitory effect on tumor growth in a drugresistant environment, which can enhance the sensitivity of chemotherapeutic drugs, suggesting that ferroptosis is very important in the treatment of tumor drug resistance, but the details are still unclear. How to use ferroptosis to fight cancer, and how to prevent drug-resistant tumor cells have become the focus and direction of research. At the end of the article, some existing problems related to ferroptosis are summarized for future research.

show abstract

“…The third major target is the selenoenzyme GPx4. Different inhibitors of GPx4 induce ferroptosis such as RLS3, FIN56, and ML210 (24) and more recently, resibufugenin (62). Postchemotherapy-"persister" cells resistant to lapatinib treatment in breast, melanoma, lung, and ovarian cancer have been characterized as GPx4-dependent (63).…”

Section: Glutathione-dependent Ferroptosismentioning

confidence: 99%

Cysteine Depletion, a Key Action to Challenge Cancer Cells to Ferroptotic Cell Death

2020

View full text Add to dashboard Cite

Cancer cells are characterized as highly proliferative at the expense of enhancement of metabolic rate. Consequently, cancer cells rely on antioxidant defenses to overcome the associated increased production of reactive oxygen species (ROS). The reliance of tumor metabolism on amino acids, especially amino acid transport systems, has been extensively studied over the past decade. Although cysteine is the least abundant amino acid in the cell, evidences described it as one of the most important amino acid for cell survival and growth. Regarding its multi-functionality as a nutrient, protein folding, and major component for redox balance due to its involvement in glutathione synthesis, disruption of cysteine homeostasis appears to be promising strategy for induction of cancer cell death. Ten years ago, ferroptosis, a new form of non-apoptotic cell death, has been described as a result of cysteine insufficiency leading to a collapse of intracellular glutathione level. In the present review, we summarized the metabolic networks involving the amino acid cysteine in cancer and ferroptosis and we focused on describing the recently discovered glutathione-independent pathway, a potential player in cancer ferroptosis resistance. Then, we discuss the implication of cysteine as key player in ferroptosis as a precursor for glutathione first, but also as metabolic precursor in glutathione-independent ferroptosis axis.

show abstract

RETRACTED: Resibufogenin inhibited colorectal cancer cell growth and tumorigenesis through triggering ferroptosis and ROS production mediated by GPX4 inactivation

Cited by 53 publications

References 31 publications

Ferroptosis in Acute Central Nervous System Injuries: The Future Direction?

Ferroptosis in Acute Central Nervous System Injuries: The Future Direction?

The Mechanism of Ferroptosis and Applications in Tumor Treatment

Cysteine Depletion, a Key Action to Challenge Cancer Cells to Ferroptotic Cell Death

Contact Info

Product

Resources

About