FIN56, a novel ferroptosis inducer, triggers lysosomal membrane permeabilization in a TFEB-dependent manner in glioblastoma

Zhang, Xin; Guo, Yulian; Li, Hao; Han, Lizhang

doi:10.7150/jca.58500

Cited by 40 publications

(30 citation statements)

References 30 publications

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“…Interestingly, the GPX4 depletor FIN56 ( Figure 4 ) was recently shown to induce ferroptosis in in vitro and in vivo GBM models ( 105 ); this was the first study to use this compound in vivo . However, the trial was not carried out with tumors in nervous tissue but rather in nude mice with subcutaneous tumors, which makes it difficult to extrapolate the possible eventual effects of FIN56 on the brain, and it is not known whether this compound can cross the blood–brain barrier to be considered a potential therapy in the future.…”

Section: Glioblastomamentioning

confidence: 98%

Pharmacological targets for the induction of ferroptosis: Focus on Neuroblastoma and Glioblastoma

et al. 2022

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Neuroblastomas are the main extracranial tumors that affect children, while glioblastomas are the most lethal brain tumors, with a median survival time of less than 12 months, and the prognosis of these tumors is poor due to multidrug resistance. Thus, the development of new therapies for the treatment of these types of tumors is urgently needed. In this context, a new type of cell death with strong antitumor potential, called ferroptosis, has recently been described. Ferroptosis is molecularly, morphologically and biochemically different from the other types of cell death described to date because it continues in the absence of classical effectors of apoptosis and does not require the necroptotic machinery. In contrast, ferroptosis has been defined as an iron-dependent form of cell death that is inhibited by glutathione peroxidase 4 (GPX4) activity. Interestingly, ferroptosis can be induced pharmacologically, with potential antitumor activity in vivo and eventual application prospects in translational medicine. Here, we summarize the main pathways of pharmacological ferroptosis induction in tumor cells known to date, along with the limitations of, perspectives on and possible applications of this in the treatment of these tumors.

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Section: Glioblastomamentioning

confidence: 98%

Pharmacological targets for the induction of ferroptosis: Focus on Neuroblastoma and Glioblastoma

et al. 2022

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“…Zhang et al. reported that FIN56 can increase lysosomal membrane permeability through a tFeb-dependent pathway and thus promote glioblastoma cell death ( 144 ).…”

Section: Caspase-independent Rcd In Targeted Therapymentioning

confidence: 99%

Application of Regulatory Cell Death in Cancer: Based on Targeted Therapy and Immunotherapy

Che

et al. 2022

Front. Immunol.

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The development of cancer treatment methods is constantly changing. For common cancers, our treatment methods are still based on conventional treatment methods, such as chemotherapy, radiotherapy, and targeted drug therapy. Nevertheless, the emergence of tumor resistance has a negative impact on treatment. Regulated cell death is a gene-regulated mode of programmed cell death. After receiving specific signal transduction, cells change their physical and chemical properties and the extracellular microenvironment, resulting in structural destruction and decomposition. As research accumulates, we now know that by precisely inducing specific cell death patterns, we can treat cancer with less collateral damage than other treatments. Many newly discovered types of RCD are thought to be useful for cancer treatment. However, some experimental results suggest that some RCDs are not sensitive to cancer cell death, and some may even promote cancer progression. This review summarizes the discovered types of RCDs, reviews their clinical efficacy in cancer treatment, explores their anticancer mechanisms, and discusses the feasibility of some newly discovered RCDs for cancer treatment in combination with the immune and tumor microenvironment.

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“…Irreversibly, the traditional ferroptotic activator (1S, 3R)-RSL3 may reduce the enzymatic activity of the Gpx4 enzyme by covalently engaging its active site selenocysteine [ 18 ]. A novel ferroptosis inducer known as FIN56 is involved in reducing the amount of Gpx4 present [ 19 ]. While the precise process is still unknown, it may have something to do with the catalase activity for acetyl-CoA carboxylase [ 20 ].…”

Section: Mechanism Of Ferroptosismentioning

confidence: 99%

Ferroptosis: A New Road towards Cancer Management

Bano¹,

Horký

Abbas

et al. 2022

Molecules

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Ferroptosis is a recently described programmed cell death mechanism that is characterized by the buildup of iron (Fe)-dependent lipid peroxides in cells and is morphologically, biochemically, and genetically distinct from other forms of cell death, having emerged to play an important role in cancer biology. Ferroptosis has significant importance during cancer treatment because of the combination of factors, including suppression of the glutathione peroxidase 4 (Gpx4), cysteine deficiency, and arachidonoyl (AA) peroxidation, which cause cells to undergo ferroptosis. However, the physiological significance of ferroptosis throughout development is still not fully understood. This current review is focused on the factors and molecular mechanisms with the diagrammatic illustrations of ferroptosis that have a role in the initiation and sensitivity of ferroptosis in various malignancies. This knowledge will open a new road for research in oncology and cancer management.

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FIN56, a novel ferroptosis inducer, triggers lysosomal membrane permeabilization in a TFEB-dependent manner in glioblastoma

Cited by 40 publications

References 30 publications

Pharmacological targets for the induction of ferroptosis: Focus on Neuroblastoma and Glioblastoma

Pharmacological targets for the induction of ferroptosis: Focus on Neuroblastoma and Glioblastoma

Application of Regulatory Cell Death in Cancer: Based on Targeted Therapy and Immunotherapy

Ferroptosis: A New Road towards Cancer Management

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