Mutation of TP53 Confers Ferroptosis Resistance in Lung Cancer Through the FOXM1/MEF2C Axis

Peng, Muyun; Hu, Qikang; Wu, Zeyu; Wang, Bin; Wang, Cheng; Yu, Fenglei

doi:10.1016/j.ajpath.2023.05.003

Cited by 5 publications

(2 citation statements)

References 39 publications

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“…On the other hand, TP53 delayed ferroptosis by upregulating its transcriptional target Cyclin-dependent kinase inhibitor 1A, which inhibited cell cycle progression and slowly consumed glutathione ( 30 ). Furthermore, TP53 mutations have been associated with increased resistance to ferroptosis in lung cancer, and this resistance is attributed to the inhibition of forkhead box M1 relieved, which in turn activates myocyte-specific enhancer factor 2C providing stress protection against ferroptosis inducers ( 31 ).…”

Section: Regulation Of Ferroptosis At Different Levels In Lung Cancermentioning

confidence: 99%

Ferroptosis in lung cancer: dual role, multi-level regulation, and new therapeutic strategies

Li,

2024

Front. Oncol.

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Lung cancer is a highly prevalent malignant tumor worldwide, with high incidence and death rates. Recently, there has been increasing recognition of the role of ferroptosis, a unique cell death mechanism, in lung cancer. This review aims to summarize the current research progress on the relationship between ferroptosis and lung cancer. It also provides a comprehensive analysis of the regulatory processes of ferroptosis in various stages, including epigenetics, transcription, post-transcription, translation, and post-translation. Additionally, the review explores the dual nature of ferroptosis in lung cancer progression, which presents interesting therapeutic possibilities. On one hand, ferroptosis can promote the escape of immune surveillance and reduce the efficacy of treatment in the early stages of tumors. On the other hand, it can counter drug resistance, enhance radiosensitivity, and promote immunotherapy. The article also discusses various combination treatment strategies based on the mechanism of ferroptosis. Overall, this review offers a holistic perspective on the role of ferroptosis in the onset, progression, and treatment of lung cancer. It aims to contribute to future research and clinical interventions in this field.

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Section: Regulation Of Ferroptosis At Different Levels In Lung Cancermentioning

confidence: 99%

Ferroptosis in lung cancer: dual role, multi-level regulation, and new therapeutic strategies

Li,

2024

Front. Oncol.

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“…In addition, pharmacological induction of ferroptosis by bioactive compounds could overcome chemotherapeutic drug resistance (Wang et al 2023), for example, targeting the STAT3-ferroptosis circuit can promote ferroptosis and restore sensitivity to chemotherapy (Ouyang et al 2022). Knockdown of FOXM1 can downregulate the expression of ferroptosis-resistant genes and increase malonaldehyde (MDA) and ROS levels in cisplatin-resistant endometrial cancer cells (Peng et al 2023). Nevertheless, the correlation between ferroptosis and FOXM1 was less reported.…”

Section: Introductionmentioning

confidence: 99%

Anticancer peptide MCP-1 induces ferroptosis in liver cancer HCCLM3 cells by targeting FOXM1/ALOXE3 signal pathway

Zhu,

Shang,

Jia

et al. 2024

Preprint

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FOXM1 is a crucial oncogenic transcription factor involved in almost all cancer hallmark pathways across all cancer types. Our previous work had found that FOXM1 targeted peptide P201 can strongly inhibit the growth of cancer cells including the liver cancer HCCLM3 cells. In addition, by RNA-seq of HCCLM3 cells treated with MCP-1, an anticancer peptide optimized from P201, ALOXE3, a key feature of ferroptosis was significantly elevated while FOXM1 was down-regulated, we wonder if the cell death of HCCLM3 induced by MCP-1 was associated with ferroptosis. Also, the relationship between FOXM1 and ferroptosis was less understood. Hence, in this study, we explore the effect of MCP-1 on ferroptosis and establish the associations among MCP-1, FOXM1 and ALOXE3 in HCCLM3 cells. The results showed that MCP-1 can significantly induce the elevated expression of ALOXE3, decreased content of GSH, down-regulation of GPX4 expression, increased contents of ROS and total iron in HCCLM3 cells. Also, ferrostatin-1, a specific inhibitor for ferroptosis, can reverse the cell death in HCCLM3 cells when co-administrated with MCP-1. TCGA database hepatocellular carcinoma gene expression analysis showed that FOXM1 was negative-related to ALOXE3 and further confirmed by the results of siRNA knockdown of FOXM1 in HCCLM3 cells. Moreover, the co-expressed genes analysis for FOXM1 and ALOXE3 revealed that many of them were closely involved in the regulation of ferroptosis. Taken together, we discovered and confirmed the induction of ferroptosis by MCP-1 in liver cancer HCCLM3 cells and primarily established the relationships among MCP-1, FOXM1 and ALOXE3.

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Heparanase accelerates the angiogenesis and inhibits the ferroptosis of p53-mutant non-small cell cancers in VEGF-dependent manner

Song,

Zhou,

Zhang

et al. 2024

Cytotechnology

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Mutation of TP53 Confers Ferroptosis Resistance in Lung Cancer Through the FOXM1/MEF2C Axis

Cited by 5 publications

References 39 publications

Ferroptosis in lung cancer: dual role, multi-level regulation, and new therapeutic strategies

Ferroptosis in lung cancer: dual role, multi-level regulation, and new therapeutic strategies

Anticancer peptide MCP-1 induces ferroptosis in liver cancer HCCLM3 cells by targeting FOXM1/ALOXE3 signal pathway

Heparanase accelerates the angiogenesis and inhibits the ferroptosis of p53-mutant non-small cell cancers in VEGF-dependent manner

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