<scp>M<sup>6</sup>A</scp> demethylase fat mass and obesity‐associated protein regulates cisplatin resistance of gastric cancer by modulating autophagy activation through <scp>ULK1</scp>

Zhang, Yan; Gao, Lei; Wang, Wen; Zhang, Teng; Dong, Fangyi; Ding, Wenping

doi:10.1111/cas.15469

Cited by 34 publications

(17 citation statements)

References 52 publications

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“…Jin et al [66] demonstrated that FTO can specifically upregulate the ULK1 protein level via m 6 A mediated demethylation, thereby promoting the activation of autophagy. Similarly, Zhang et al also reported that FTO promotes cisplatin resistance by facilitating autophagy by targeting ULK1 via an m 6 A-dependent manner in gastric cancer cells [67]. Moreover, the downregulation of FTO suppressed the expression of ATG5 and ATG7, inhibiting autophagosome formation, thereby restaining autophagy and adipogenesis [68].…”

Section: Ftomentioning

confidence: 91%

Novel Insights into The Roles of N⁶-methyladenosine (m⁶A) Modification and Autophagy in Human Diseases

et al. 2023

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Autophagy is an evolutionarily conserved cellular degradation and recycling process. It is important for maintaining vital cellular function and metabolism. Abnormal autophagy activity can cause the development of various diseases. N 6 -methyladenosine (m 6 A) methylation is the most prevalent and abundant internal modification in eukaryotes, affecting almost all aspects of RNA metabolism. The process of m 6 A modification is dynamic and adjustable. Its regulation depends on the regulation of m 6 A methyltransferases, m 6 A demethylases, and m 6 A binding proteins. m 6 A methylation and autophagy are two crucial and independent cellular events. Recent studies have shown that m 6 A modification mediates the transcriptional and post-transcriptional regulation of autophagy-related genes, affecting autophagy regulatory networks in multiple diseases. However, the regulatory effects of m 6 A regulators on autophagy in human diseases are not adequately acknowledged. In the present review, we summarized the latest knowledge of m 6 A modification in autophagy and elucidated the molecular regulatory mechanisms underlying m 6 A modification in autophagy regulatory networks. Moreover, we discuss the potentiality of m 6 A regulators serving as promising predictive biomarkers for human disease diagnosis and targets for therapy. This review will increase our understanding of the relationship between m 6 A methylation and autophagy, and provide novel insights to specifically target m 6 A modification in autophagy-associated therapeutic strategies.

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Section: Ftomentioning

confidence: 91%

Novel Insights into The Roles of N⁶-methyladenosine (m⁶A) Modification and Autophagy in Human Diseases

et al. 2023

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“…Thus, METTL3 inhibits autophagy to enhance anticancer drug sensitivity. The expression of FTO was increased in cisplatin-resistant (SGC-7901/DDP) gastric cancer cells [ 166 ]. The downregulation of FTO reversed cisplatin resistance in SGC-7901/DDP cells, which was attributed to the inhibition of (ULK1)-mediated autophagy ( Figure 3 C) [ 166 ].…”

Section: The Roles Of Mettl3 In Anticancer Drug Resistance and Autophagymentioning

confidence: 99%

“…The expression of FTO was increased in cisplatin-resistant (SGC-7901/DDP) gastric cancer cells [ 166 ]. The downregulation of FTO reversed cisplatin resistance in SGC-7901/DDP cells, which was attributed to the inhibition of (ULK1)-mediated autophagy ( Figure 3 C) [ 166 ]. Thus, high levels of m6A enhance the sensitivity of cancer cells to cisplatin by inhibiting autophagy.…”

Section: The Roles Of Mettl3 In Anticancer Drug Resistance and Autophagymentioning

confidence: 99%

Roles of RNA Methylations in Cancer Progression, Autophagy, and Anticancer Drug Resistance

Shim

Jeoung

2023

IJMS

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RNA methylations play critical roles in RNA processes, including RNA splicing, nuclear export, nonsense-mediated RNA decay, and translation. Regulators of RNA methylations have been shown to be differentially expressed between tumor tissues/cancer cells and adjacent tissues/normal cells. N6-methyladenosine (m6A) is the most prevalent internal modification of RNAs in eukaryotes. m6A regulators include m6A writers, m6A demethylases, and m6A binding proteins. Since m6A regulators play important roles in regulating the expression of oncogenes and tumor suppressor genes, targeting m6A regulators can be a strategy for developing anticancer drugs. Anticancer drugs targeting m6A regulators are in clinical trials. m6A regulator-targeting drugs could enhance the anticancer effects of current chemotherapy drugs. This review summarizes the roles of m6A regulators in cancer initiation and progression, autophagy, and anticancer drug resistance. The review also discusses the relationship between autophagy and anticancer drug resistance, the effect of high levels of m6A on autophagy and the potential values of m6A regulators as diagnostic markers and anticancer therapeutic targets.

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“…Autophagy is an auto‐catabolic process that permits cells to deal with stress‐coping strategies by degrading damaged organelles and accumulated proteins, which could result in cancer resistance treated with anticancer drugs 85–89 . LncRNA regulates cell autophagy and contributes to chemoresistance.…”

Section: Mechanisms Underlying Cancer Drug Resistancementioning

confidence: 99%

New insights into the interaction between m6A modification and lncRNA in cancer drug resistance

Jin,

Fan

2023

Cell Proliferation

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Drug resistance is perhaps the greatest obstacle in improving outcomes for cancer patients, leading to recurrence, progression and metastasis of various cancers. Exploring the underlying mechanism worth further study. N6‐methyladenosine (m6A) is the most common RNA modification found in eukaryotes, playing a vital role in RNA translation, transportation, stability, degradation, splicing and processing. Long noncoding RNA (lncRNA) refers to a group of transcripts that are longer than 200 nucleotides (nt) and typically lack the ability to code for proteins. LncRNA has been identified to play a significant role in regulating multiple aspects of tumour development and progression, including proliferation, metastasis, metabolism, and resistance to treatment. In recent years, a growing body of evidence has emerged, highlighting the crucial role of the interplay between m6A modification and lncRNA in determining the sensitivity of cancer cells to chemotherapeutic agents. In this review, we focus on the recent advancements in the interaction between m6A modification and lncRNA in the modulation of cancer drug resistance. Additionally, we aim to explore the underlying mechanisms involved in this process. The objective of this review is to provide valuable insights and suggest potential future directions for the reversal of chemoresistance in cancer.

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M⁶A demethylase fat mass and obesity‐associated protein regulates cisplatin resistance of gastric cancer by modulating autophagy activation through ULK1

Cited by 34 publications

References 52 publications

Novel Insights into The Roles of N⁶-methyladenosine (m⁶A) Modification and Autophagy in Human Diseases

Novel Insights into The Roles of N⁶-methyladenosine (m⁶A) Modification and Autophagy in Human Diseases

Roles of RNA Methylations in Cancer Progression, Autophagy, and Anticancer Drug Resistance

New insights into the interaction between m6A modification and lncRNA in cancer drug resistance

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M6A demethylase fat mass and obesity‐associated protein regulates cisplatin resistance of gastric cancer by modulating autophagy activation through ULK1

Cited by 34 publications

References 52 publications

Novel Insights into The Roles of N6-methyladenosine (m6A) Modification and Autophagy in Human Diseases

Novel Insights into The Roles of N6-methyladenosine (m6A) Modification and Autophagy in Human Diseases

Roles of RNA Methylations in Cancer Progression, Autophagy, and Anticancer Drug Resistance

New insights into the interaction between m6A modification and lncRNA in cancer drug resistance

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M⁶A demethylase fat mass and obesity‐associated protein regulates cisplatin resistance of gastric cancer by modulating autophagy activation through ULK1

Novel Insights into The Roles of N⁶-methyladenosine (m⁶A) Modification and Autophagy in Human Diseases

Novel Insights into The Roles of N⁶-methyladenosine (m⁶A) Modification and Autophagy in Human Diseases