Inhibitory effect of hydnocarpin D on T-cell acute lymphoblastic leukemia via induction of autophagy-dependent ferroptosis

Lou, Siyue; Hong, Huanwu; Maihesuti, Liwaliding; Gao, Hang; Zhu, Zhihui; Xu, Lili; Tian, Shasha; Kai, Guoyin; Huang, Guozheng; Zhao, Huajun

doi:10.1177/15353702211004870

Cited by 14 publications

(11 citation statements)

References 36 publications

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“…The above studies have shown that ALL is highly sensitive to ferroptosis ( 103 – 107 ), accompanied by excessive accumulation of ROS and increased lipid peroxidation level, which is consistent with the currently known classical pathway of ferroptosis. Overall, these studies offer novel insight into the molecular regulatory mechanisms of ferroptosis and may contribute to developing new therapeutic strategies to reactivate programmed cell death in ALL.…”

Section: Application Of Ferroptosis In Hematologic Malignanciessupporting

confidence: 85%

“…Hynocarpin D (HD) is a bioactive flavonoid lignin compound with good antitumor activity but insufficient understanding of its mechanism. Lou et al ( 103 ) found that in T-cell acute lymphoblastic leukemia (T-ALL) cell lines Jurkat and Molt-4, HD could inhibit the proliferation of T-ALL by inducing cell cycle arrest and subsequent apoptosis. In addition, HD could also increase LC3-II levels and the formation of autophagy lysosomal vacuoles, both of which are markers of autophagy.…”

Section: Application Of Ferroptosis In Hematologic Malignanciesmentioning

confidence: 99%

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Molecular Mechanisms of Ferroptosis and Its Roles in Hematologic Malignancies

2021

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Cell death is essential for the normal metabolism of human organisms. Ferroptosis is a unique regulated cell death (RCD) mode characterized by excess accumulation of iron-dependent lipid peroxide and reactive oxygen species (ROS) compared with other well-known programmed cell death modes. It has been currently recognized that ferroptosis plays a rather important role in the occurrence, development, and treatment of traumatic brain injury, stroke, acute kidney injury, liver damage, ischemia–reperfusion injury, tumor, etc. Of note, ferroptosis may be explained by the expression of various molecules and signaling components, among which iron, lipid, and amino acid metabolism are the key regulatory mechanisms of ferroptosis. Meanwhile, tumor cells of hematological malignancies, such as leukemia, lymphoma, and multiple myeloma (MM), are identified to be sensitive to ferroptosis. Targeting potential regulatory factors in the ferroptosis pathway may promote or inhibit the disease progression of these malignancies. In this review, a systematic summary was conducted on the key molecular mechanisms of ferroptosis and the current potential relationships of ferroptosis with leukemia, lymphoma, and MM. It is expected to provide novel potential therapeutic approaches and targets for hematological malignancies.

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Section: Application Of Ferroptosis In Hematologic Malignanciessupporting

confidence: 85%

Section: Application Of Ferroptosis In Hematologic Malignanciesmentioning

confidence: 99%

Molecular Mechanisms of Ferroptosis and Its Roles in Hematologic Malignancies

2021

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“…Typhaneoside, a flavonoid extracted from Pollen typhae , has also been reported to induce apoptosis and ferroptosis associated with ferritinophagy in AML cells [ 195 ]. Hydnocarpin D is another flavonoid demonstrated to induce apoptosis and ferroptosis through autophagy in ALL cells [ 196 ]. Perillaldehyde, the main component of Ammodaucus leucotrichus , downregulates GSH and GPX4 to induce ferroptosis in HL-60 cells and primary AML cells [ 197 ].…”

Section: Ferroptosis In Leukemiamentioning

confidence: 99%

Molecular Mechanisms of Ferroptosis and Updates of Ferroptosis Studies in Cancers and Leukemia

Akiyama

Carter

Andreeff

et al. 2023

Cells

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Ferroptosis is a mode of cell death regulated by iron-dependent lipid peroxidation. Growing evidence suggests ferroptosis induction as a novel anti-cancer modality that could potentially overcome therapy resistance in cancers. The molecular mechanisms involved in the regulation of ferroptosis are complex and highly dependent on context. Therefore, a comprehensive understanding of its execution and protection machinery in each tumor type is necessary for the implementation of this unique cell death mode to target individual cancers. Since most of the current evidence for ferroptosis regulation mechanisms is based on solid cancer studies, the knowledge of ferroptosis with regard to leukemia is largely lacking. In this review, we summarize the current understanding of ferroptosis-regulating mechanisms with respect to the metabolism of phospholipids and iron as well as major anti-oxidative pathways that protect cells from ferroptosis. We also highlight the diverse impact of p53, a master regulator of cell death and cellular metabolic processes, on the regulation of ferroptosis. Lastly, we discuss recent ferroptosis studies in leukemia and provide a future perspective for the development of promising anti-leukemia therapies implementing ferroptosis induction.

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“…Moreover, this cytotoxic autophagy caused ferroptosis, which was characterized by the accumulation of lipid ROS and a decrease in GSH and GPX4, and conversely, inhibition of autophagy hindered cell ferroptosis. [ 166 ] Soyauxinium chloride (SCHL) is a naturally occurring indole-quinazoline-type alkaloid. Some studies found that SCHL induced cytotoxicity of CCRF-CEM leukemia cells through caspase 3, 7, 8, and 9 activation, MMP alteration, and increased ROS generation, while the presence of Fer-1 (ferrostain-1) or DFA (deferoxamine; an iron-related death inhibitor) decreased SCHL cytotoxicity by 7.11- and 4.64-fold, respectively, indicating that SCHL is involved in ferroptosis.…”

Section: Recent Advances Of Ferroptosis In Almentioning

confidence: 99%

Ferroptosis in Acute Leukemia

Lyu

Song

2023

Chinese Medical Journal

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Ferroptosis is an iron-dependent cell death pathway that is different from apoptosis, pyroptosis, and necrosis. The main characteristics of ferroptosis are the Fenton reaction mediated by intracellular free divalent iron ions, lipid peroxidation of cell membrane lipids, and inhibition of the anti-lipid peroxidation activity of intracellular glutathione peroxidase 4 (GPX4). Recent studies have shown that ferroptosis can be involved in the pathological processes of many disorders, such as ischemiareperfusion injury, nervous system diseases, and blood diseases. However, the specific mechanisms by which ferroptosis participates in the occurrence and development of acute leukemia still need to be more fully and deeply studied. This article reviews the characteristics of ferroptosis and the regulatory mechanisms promoting or inhibiting ferroptosis. More importantly, it further discusses the role of ferroptosis in acute leukemia and predicts a change in treatment strategy brought about by increased knowledge of the role of ferroptosis in acute leukemia.

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Inhibitory effect of hydnocarpin D on T-cell acute lymphoblastic leukemia via induction of autophagy-dependent ferroptosis

Cited by 14 publications

References 36 publications

Molecular Mechanisms of Ferroptosis and Its Roles in Hematologic Malignancies

Molecular Mechanisms of Ferroptosis and Its Roles in Hematologic Malignancies

Molecular Mechanisms of Ferroptosis and Updates of Ferroptosis Studies in Cancers and Leukemia

Ferroptosis in Acute Leukemia

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