Typhaneoside prevents acute myeloid leukemia (AML) through suppressing proliferation and inducing ferroptosis associated with autophagy

Zhu, Haiyan; Huang, Zhenguang; Chen, Guoqi; Sheng, Fen; Zheng, Yin-Suo

doi:10.1016/j.bbrc.2019.06.070

Cited by 60 publications

(49 citation statements)

References 34 publications

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“…Amentoflavone represses the expression of FTH by autophagy via activation of the AMPK/mTOR/p70S6K signaling pathway to trigger in vitro and in vivo ferroptosis in an autophagy-dependent manner ( 177 ). Typhaneoside, a major flavonoid found in the extract of Pollen Typhae , promotes the activation of the AMPK signaling pathway to contribute to ferritin degradation, ROS accumulation, and ferroptosis in Kas-1, HL-60, and NB4 cells ( 202 ). Pseudolaric acid B isolated from cortex pseudolaricis triggers ferroptosis in vivo and in vitro by upregulating TFR1, activating NOX4, and inhibiting SLC7A11 ( 178 ).…”

Section: Ferroptosis and Cancermentioning

confidence: 99%

Ferroptosis: Biochemistry and Biology in Cancers

et al. 2021

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The challenge of eradicating cancer is that cancer cells possess diverse mechanisms to protect themselves from clinical strategies. Recently, ferroptosis has been shown to exhibit appreciable anti-tumor activity that could be harnessed for cancer therapy in the future. Ferroptosis is an iron-dependent form of regulated cell death that is characterized by the oxidization of polyunsaturated fatty acids (PUFAs) and accumulation of lipid peroxides. Ferroptosis has been closely correlated with numerous biological processes, such as amino acid metabolism, glutathione metabolism, iron metabolism, and lipid metabolism, as well as key regulators including GPX4, FSP1, NRF2, and p53. Although ferroptosis could be involved in killing various cancer cells, multiple aspects of this phenomenon remain unresolved. In this review, we summarize the biochemistry and biology of ferroptosis in diverse cancers and discuss the potential mechanisms of ferroptosis, which might pave the way for guiding cancer therapeutics.

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Section: Ferroptosis and Cancermentioning

confidence: 99%

Ferroptosis: Biochemistry and Biology in Cancers

et al. 2021

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“…Due to their high metabolic characteristics, most tumours are in a state of high oxidative stress and are required to increase their ROS scavenging ability to prevent oxidative damage, which may make them sensitive to ferroptosis [14]. Many cancers have been proven to be ferroptosis-related, such as hepatocellular carcinoma [15], gastric cancer [16,17], ovarian cancer [18,19], and breast cancer [20,21]. Therefore, inducing ferroptosis to promote cell death or inhibit cell growth for cancer could be a new therapeutic strategy [22].…”

Section: Introductionmentioning

confidence: 99%

A novel ferroptosis-related 12-gene signature predicts clinical prognosis and reveals immune relevancy in clear cell renal cell carcinoma

Hong

Lin

et al. 2021

BMC Cancer

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Background Clear cell renal cell carcinoma (ccRCC) is still highly aggressive and lethal even with various therapeutic approaches. As the kidney is an iron metabolism-related organ, exploring and assessing the clinical value of ferroptosis, an iron-dependent regulated cell death, is practical and important. Methods Prognostic ferroptosis-related differentially expressed genes (DEGs) were identified from the KIRC cohort in the cancer genome atlas (TCGA) database, from which a prognostic signature was established using Lasso-penalized Cox regression analysis. Each patient in the KIRC cohort and the E-MTAB-1980 cohort (from the ArrayExpress database) was assigned a calculated signature-correlated risk score and categorized to be either in the high- or low-risk group divided by the median risk score in the KIRC cohort. Then, the independent prognostic value of the signature was further assessed by Kaplan-Meier (K-M) survival, time-dependent receiver operating characteristic (ROC) and Cox regression analyses based on overall survival (OS) in both cohorts. Finally, risk-related DEGs were identified in both cohorts and subjected to enrichment analyses for Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG) and immune infiltration. Results Among 60 ferroptosis-related genes, 32 prognostic DEGs were identified, from which we constructed a prognostic 12-gene signature with CARS1, HMGCR, CHAC1, GOT1, CD44, STEAP3, AKR1C1, CBS, DPP4, FANCD2, SLC1A5 and NCOA4. Patients in both cohorts were divided into high- and low-risk groups, which were visually distributed in two sets and had positive-risk-related mortality. The K-M survival and the ROC curves validated that the signature has prognostic value with P < 0.05 and area under the curve > 0.7 in both cohorts, respectively. Multivariate Cox regression further confirmed the risk score as an independent prognostic predictor for OS. Commonly enriched terms in GO and KEGG not only showed a high iron correlation but also, interestingly, immune relevance of 3 immune cells (macrophages, mast cells and regulatory T cells) and 1 immune-related function (antigen processing cell co-stimulation). Conclusion We established a novel 12 ferroptosis-related-gene signature that was proven to be an independent prognostic predictor for OS and inferred to be related to tumour immunity in ccRCC; however, the underlying mechanism is still poorly characterized and needs further exploration.

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“…AMPK could also regulate mitochondrial homeostasis [ 19 ], and discovering mitochondria-independent mechanisms that inhibit ferroptosis has great implications. Additionally, AMPK activation causes the degradation of ferritin (Fer), accumulation of ROS, and activation of ferroptosis [ 20 , 21 ]. A study suggested that AMPK is an upstream regulator of ferroptosis, and AMPK depletion sensitizes cells to ferroptosis [ 22 ]; however, due to insufficient detection of ferroptosis-related biomarkers and lack of mitochondrial phenotype support, the specific regulatory effect of AMPK on ferroptosis remains obscure.…”

Section: The Characteristics Of Ferroptosismentioning

confidence: 99%

The Cross‐Link between Ferroptosis and Kidney Diseases

Wang

Liu

Wang

et al. 2021

Oxidative Medicine and Cellular Longevity

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Acute and chronic kidney injuries result from structural dysfunction and metabolic disorders of the kidney in various etiologies, which significantly affect human survival and social wealth. Nephropathies are often accompanied by various forms of cell death and complex microenvironments. In recent decades, the study of kidney diseases and the traditional forms of cell death have improved. Nontraditional forms of cell death, represented by ferroptosis and necroptosis, have been discovered in the field of kidney diseases, which have reshuffled the role of traditional cell death in nephropathies. Although interactions between ferroptosis and acute kidney injury (AKI) have been continuously explored, studies on ferroptosis and chronic kidney disease (CKD) remain limited. Here, we have reviewed the therapeutic significance of ferroptosis in AKI and anticipated the curative potential of ferroptosis for CKD in the hope of providing insights into ferroptosis and CKD.

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Typhaneoside prevents acute myeloid leukemia (AML) through suppressing proliferation and inducing ferroptosis associated with autophagy

Cited by 60 publications

References 34 publications

Ferroptosis: Biochemistry and Biology in Cancers

Ferroptosis: Biochemistry and Biology in Cancers

A novel ferroptosis-related 12-gene signature predicts clinical prognosis and reveals immune relevancy in clear cell renal cell carcinoma

The Cross‐Link between Ferroptosis and Kidney Diseases

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