ARNTL2 is an indicator of poor prognosis, promotes epithelial-to-mesenchymal transition and inhibits ferroptosis in lung adenocarcinoma

Zhang, Huan; Shan, Guangyao; Jin, Xing; Yu, Xiangyang; Bi, Guoshu; Feng, Mingxiang; Wang, Hao; Lin, Miao; Zhan, Cheng; Wang, Qun; Li, Ming

doi:10.1016/j.tranon.2022.101562

Cited by 8 publications

(4 citation statements)

References 40 publications

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“…However, there is also a negative feedback loop between EMT and ferroptosis. High ARNTL2 expression was associated with EMT and lymph node metastasis in patients with LUAD, while it plays an inhibiting role in ferroptosis [41].…”

Section: Ferroptosis In Luad Progressionmentioning

confidence: 94%

“…As a first example, the aryl hydrocarbon receptor nuclear translocator like 2 (ARNTL2), as a circadian transcription factor, increases the expression of acyl-CoA thioesterase 7 (ACOT7) via binding to the ACOT7 promoter, which in turn promotes the synthesis of MUFAs such as oleic acid and palmitoleic acid [79]. Given that ARNTL2 promotes EMT and cell proliferation and migration in addition to inhibiting lipid peroxidation and ferroptosis via ACOT7, ARNTL2 may be a poor biomarker for LUAD [41]. As a second example, cAMP response element-binding protein (CREB) and kruppel-like factor 11 (KLF11) can promote or repress GPX4 expression by binding to the GPX4 promoter, respectively.…”

Section: Othersmentioning

confidence: 99%

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Regulation of Ferroptosis in Lung Adenocarcinoma

Wei,

Li,

et al. 2023

IJMS

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Lung adenocarcinoma (LUAD) is the most common lung cancer, which accounts for about 35–40% of all lung cancer patients. Despite therapeutic advancements in recent years, the overall survival time of LUAD patients still remains poor, especially KRAS mutant LUAD. Therefore, it is necessary to further explore novel targets and drugs to improve the prognos is for LUAD. Ferroptosis, an iron-dependent regulated cell death (RCD) caused by lipid peroxidation, has attracted much attention recently as an alternative target for apoptosis in LUAD therapy. Ferroptosis has been found to be closely related to LUAD at every stage, including initiation, proliferation, and progression. In this review, we will provide a comprehensive overview of ferroptosis mechanisms, its regulation in LUAD, and the application of targeting ferroptosis for LUAD therapy.

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Section: Ferroptosis In Luad Progressionmentioning

confidence: 94%

Section: Othersmentioning

confidence: 99%

Regulation of Ferroptosis in Lung Adenocarcinoma

Wei,

Li,

et al. 2023

IJMS

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“…Inhibition of ferroptosis promotes epithelial-mesenchymal transition of cancer cells, leading to cancer migration, metastasis and poor prognosis. Both ferroptosis inhibition and EMT induction occurr in IRF2 overexpressed glioma cells and ARNTL2 overexpressed lung adenocarcinoma cells, which also suggest poor prognosis of both kinds of cancer [39]. Mechanistically, Some processes related with ferroptosis like ferritinophagy and ROS production were found to be involved in drug-induced EMT inhibition in hepatocellular carcinoma [40] and gastric cancer cell lines [41], and the inhibition of EMT was reversed with the Fer-1, a ferroptosis inhibitor.…”

Section: Ferroptosis and Emt In Cancermentioning

confidence: 97%

Ferroptosis in Cancer Progression

Zhang¹,

Chen²,

Wang³

et al. 2023

Preprint

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Ferroptosis is a newly discovered iron-dependent form of regulated cell death driven by phospholipid peroxidation, associated with processes including iron overload, lipid peroxidation and dysfunction of cellular antioxidant systems. Ferroptosis is found closely related to many diseases including cancer, at its every stage. Epithelial-mesenchymal transition (EMT) in malignant tumors that originate from epithelia promotes cancer cell migration, invasion and metastasis by disrupting cell-cell and cell-martrix junctions, cell polarity, etc. Recent studies have shown that ferroptosis appears to share multiple initiators and overlapping pathways with EMT in cancers and identify ferroptosis as a potential predictor of various cancer grade and prognosis. Cancer metastasis involves multiple steps including local invasion of cancer cells, intravasation, survival in circulation, arrest at a distant organ site, extravasation and adaptation to foreign tissue microenvironments, angiogenesis and the formation of “premetastatic niche”. Numerous studies have revealed that ferroptosis is closely associated with cancer metastasis. From the cellular perspective, ferroptosis has been implicated in the regulation of cancer metastasis. From the molecular perspective, the signaling pathways activated during the two events interweave. This review briefly introduces the mechanisms of ferroptosis, and discusses how ferroptosis is involved in cancer progression including EMT, cancer angiogenesis, invasion and metastasis.

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“…Inhibition of ferroptosis promotes epithelial-mesenchymal transition of cancer cells, leading to cancer migration, metastasis, and poor prognosis. Both ferroptosis inhibition and EMT induction occur in IRF2 overexpressed glioma cells and ARNTL2 overexpressed lung adenocarcinoma cells, which also suggests poor prognosis for both kinds of cancer [39]. Mechanistically, some processes related to ferroptosis such as ferritinophagy and ROS production were found to be involved in drug-induced EMT inhibition in hepatocellular carcinoma [40] and gastric cancer cell lines [41]; the inhibition of EMT was reversed with the Fer-1, a ferroptosis inhibitor.…”

Section: Ferroptosis and Emt In Cancermentioning

confidence: 97%

Ferroptosis in Cancer Progression

Zhang

Chen

Wang

et al. 2023

Cells

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Ferroptosis is a newly discovered iron-dependent form of regulated cell death driven by phospholipid peroxidation and associated with processes including iron overload, lipid peroxidation, and dysfunction of cellular antioxidant systems. Ferroptosis is found to be closely related to many diseases, including cancer at every stage. Epithelial–mesenchymal transition (EMT) in malignant tumors that originate from epithelia promotes cancer-cell migration, invasion, and metastasis by disrupting cell–cell and cell–cell matrix junctions, cell polarity, etc. Recent studies have shown that ferroptosis appears to share multiple initiators and overlapping pathways with EMT in cancers and identify ferroptosis as a potential predictor of various cancer grades and prognoses. Cancer metastasis involves multiple steps, including local invasion of cancer cells, intravasation, survival in circulation, arrest at a distant organ site, extravasation and adaptation to foreign tissue microenvironments, angiogenesis, and the formation of “premetastatic niche”. Numerous studies have revealed that ferroptosis is closely associated with cancer metastasis. From the cellular perspective, ferroptosis has been implicated in the regulation of cancer metastasis. From the molecular perspective, the signaling pathways activated during the two events interweave. This review briefly introduces the mechanisms of ferroptosis and discusses how ferroptosis is involved in cancer progression, including EMT, cancer angiogenesis, invasion, and metastasis.

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ARNTL2 is an indicator of poor prognosis, promotes epithelial-to-mesenchymal transition and inhibits ferroptosis in lung adenocarcinoma

Cited by 8 publications

References 40 publications

Regulation of Ferroptosis in Lung Adenocarcinoma

Regulation of Ferroptosis in Lung Adenocarcinoma

Ferroptosis in Cancer Progression

Ferroptosis in Cancer Progression

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