Downregulation of miR-221–3p promotes the ferroptosis in gastric cancer cells via upregulation of ATF3 to mediate the transcription inhibition of GPX4 and HRD1

Shao, Chang-Jiang; Zhou, Hai-Lang; Gao, Xu-Zhu; Xu, Chun-Fang

doi:10.1016/j.tranon.2023.101649

Cited by 15 publications

(7 citation statements)

References 52 publications

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“…Upregulated ATF3 can inhibit the transcription of GPX4 and HRD1, further suppressing the proliferation of GC cells. HRD1 itself can inhibit ferroptosis by mediating the ubiquitination and degradation of ACSL4 ( Shao et al, 2023 ). Moreover, miR-103a-3p has been found to be highly expressed in GC cells and promotes their proliferation.…”

Section: The Regulatory Mechanisms Of Ferroptosis In Gc Cellsmentioning

confidence: 99%

“…Glutaminase 2 (GLS2), targeted by miR-103a-3p, can be downregulated to inhibit GC cell proliferation and promote ferroptosis (Hu et al, 2018;Wu et al, 2020). Furthermore, in the previously mentioned miR-221-3p/ ATF3 pathway, ATF3 has been identified as a downstream mRNA target of miR-221-3p (Shao et al, 2023). Relevant studies have confirmed that miRNAs can regulate mRNA through binding to the 3′untranslated region and can interact with other non-coding RNAs to mutually regulate ferroptosis in GC cells (Mao et al, 2017) (Figure 3).…”

Section: Non-codingmentioning

confidence: 99%

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Ferroptosis and its current progress in gastric cancer

Yue,

Yuan,

Zhou

et al. 2024

Front. Cell Dev. Biol.

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Gastric Cancer (GC) is a prevalent malignancy within the digestive tract, ranking as the fifth most common malignant tumor worldwide. It is characterized by clinical features such as a tendency for metastasis and an unfavorable prognosis. Ferroptosis, a recently identified form of cell death, represents a novel mode of cellular demise that diverges from the traditional concepts of necrosis and apoptosis. Numerous studies have found that ferroptosis plays a significant role in the proliferation, metastasis, drug resistance, and microenvironment regulation within GC. This review summarizes the mechanism of ferroptosis and its role in the occurrence and development of GC cells. It provides examples demonstrating how various anti-tumor drugs can induce ferroptosis in GC cells. Additionally, it summarizes the potential application value of ferroptosis in the future treatment of GC.

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Section: The Regulatory Mechanisms Of Ferroptosis In Gc Cellsmentioning

confidence: 99%

Section: Non-codingmentioning

confidence: 99%

Ferroptosis and its current progress in gastric cancer

Yue,

Yuan,

Zhou

et al. 2024

Front. Cell Dev. Biol.

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“…ATF3 mediates osteoblast ferroptosis by inhibiting the expression of GPX4 and promoting the accumulation of lipid peroxides [105]. ATF3 induces ferroptosis in GC cells by transcriptionally repressing GPX4 and HRD1 [111]. HRD1 mediates the ubiquitination and degradation of ACSL4 to inhibit ferroptosis [111].…”

Section: The Regulation Of Ferroptosismentioning

confidence: 99%

“…ATF3 induces ferroptosis in GC cells by transcriptionally repressing GPX4 and HRD1 [111]. HRD1 mediates the ubiquitination and degradation of ACSL4 to inhibit ferroptosis [111]. ACSL4 is a key molecule that promotes the ferroptosis process [112,113].…”

Section: The Regulation Of Ferroptosismentioning

confidence: 99%

The Dual Roles of Activating Transcription Factor 3 (ATF3) in Inflammation, Apoptosis, Ferroptosis, and Pathogen Infection Responses

Liu,

Li,

Lan

et al. 2024

IJMS

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Transcription factors are pivotal regulators in the cellular life process. Activating transcription factor 3 (ATF3), a member of the ATF/CREB (cAMP response element-binding protein) family, plays a crucial role as cells respond to various stresses and damage. As a transcription factor, ATF3 significantly influences signal transduction regulation, orchestrating a variety of signaling pathways, including apoptosis, ferroptosis, and cellular differentiation. In addition, ATF3 serves as an essential link between inflammation, oxidative stress, and immune responses. This review summarizes the recent advances in research on ATF3 activation and its role in regulating inflammatory responses, cell apoptosis, and ferroptosis while exploring the dual functions of ATF3 in these processes. Additionally, this article discusses the role of ATF3 in diseases related to pathogenic microbial infections. Our review may be helpful to better understand the role of ATF3 in cellular responses and disease progression, thus promoting advancements in clinical treatments for inflammation and oxidative stress-related diseases.

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“…Activation of transcription factor 2 (ATF2) knockdown promotes sorafenib-induced ferroptosis by decreasing the stability of SLC7A11 by reducing interaction of HSPH1 with SLC7A11 [ 102 ]. Activated transcription factor 3 (ATF3) promotes ferroptosis and inhibits GC cell proliferation by down-regulating GPX4 and HRD1 transcription [ 103 ]. Moreover, ATF3 blocks the Nrf2/Keap1/xCT signaling pathway, promoting the sensitivity of GC cells to the chemotherapeutic drug cisplatin [ 104 ].…”

Section: Ferroptosis and Gcmentioning

confidence: 99%

Ferroptosis and its role in gastric and colorectal cancers

Hou,

Wang,

et al. 2024

Korean J Physiol Pharmacol

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Ferroptosis is a novel mechanism of programmed cell death, characterized by intracellular iron overload, intensified lipid peroxidation, and abnormal accumulation of reactive oxygen species, which ultimately resulting in cell membrane impairment and demise. Research has revealed that cancer cells exhibit a greater demand for iron compared to normal cells, indicating a potential susceptibility of cancer cells to ferroptosis. Stomach and colorectal cancers are common gastrointestinal malignancies, and their elevated occurrence and mortality rates render them a global health concern. Despite significant advancements in medical treatments, certain unfavorable consequences and drug resistance persist. Consequently, directing attention towards the phenomenon of ferroptosis in gastric and colorectal cancers holds promise for enhancing therapeutic efficacy. This review aims to elucidate the intricate cellular metabolism associated with ferroptosis, encompassing lipid and amino acid metabolism, as well as iron metabolic processes. Furthermore, the significance of ferroptosis in the context of gastric and colorectal cancer is thoroughly examined and discussed.

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Downregulation of miR-221–3p promotes the ferroptosis in gastric cancer cells via upregulation of ATF3 to mediate the transcription inhibition of GPX4 and HRD1

Cited by 15 publications

References 52 publications

Ferroptosis and its current progress in gastric cancer

Ferroptosis and its current progress in gastric cancer

The Dual Roles of Activating Transcription Factor 3 (ATF3) in Inflammation, Apoptosis, Ferroptosis, and Pathogen Infection Responses

Ferroptosis and its role in gastric and colorectal cancers

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