Role of ferroptosis and ferroptosis-related non-coding RNAs in the occurrence and development of gastric cancer

Lü, Ling; Chen, Bei; Xu, Yumeng; Zhang, Xinyi; Jin, Longtao; Qian, Hui; Wang, Yi; Zhao, Liang

doi:10.3389/fphar.2022.902302

Cited by 8 publications

(9 citation statements)

References 53 publications

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“…Gastric cancer, also known as stomach cancer, is a relatively common malignancy, being the third most common cause of cancer-related deaths worldwide (Lu et al 2022 ; Ma et al 2022 ). With a relative five-year survival rate below 30% in its advanced stage, it has a poor prognosis and represents a substantial socio-medical burden that remains to be addressed (Yu et al 2023 ).…”

Section: Introductionmentioning

confidence: 99%

Helicobacter pylori upregulates circPGD and promotes development of gastric cancer

Zhao,

Yao,

Cao

et al. 2024

J Cancer Res Clin Oncol

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Purpose Helicobacter pylori (H. pylori) has unique biochemical traits and pathogenic mechanisms, which make it a substantial cause of gastrointestinal cancers. Circular RNAs (circRNAs) have concurrently been identified as an important participating factor in the pathophysiology of several different cancers. However, the underlying processes and putative interactions between H. pylori and circRNAs have received very little attention. To address this issue, we explored the interaction between H. pylori and circRNAs to investigate how they might jointly contribute to the occurrence and development of gastric cancer. Methods Changes in circPGD expression in H. pylori were detected using qRT-PCR. Cell proliferation and migration changes were assayed by colony formation, the CCK-8 assay and the transwell assay. Apoptosis was measured by flow cytometry. Western blot was conducted to detect changes in cell migration, apoptosis, proliferation and inflammation-associated proteins. QRT-PCR was used to measure changes in circPGD and inflammation-associated factors. Results We found that H. pylori induced increased circPGD expression in infected human cells and facilitated gastric cancer progression in three ways by promoting cell proliferation and migration, enhancing the inflammatory response, and inhibiting apoptosis. Conclusions CircPGD appears to play a role in H. pylori-related gastric cancer and may thus be a viable, novel target for therapeutic intervention.

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Section: Introductionmentioning

confidence: 99%

Helicobacter pylori upregulates circPGD and promotes development of gastric cancer

Zhao,

Yao,

Cao

et al. 2024

J Cancer Res Clin Oncol

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“…Delving deeper into exploring the pathogenesis of GC holds a guiding significance for the treatment of later-stage GC. Ferroptosis, an iron-dependent form of programmed cell death characterized by lipid peroxidation accumulation, intricately regulates the biological processes of malignancies ( Lu et al, 2022 ). Various studies have demonstrated that ferroptosis plays a crucial role in GC’s occurrence, progression, treatment, and prognosis.…”

Section: Introductionmentioning

confidence: 99%

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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“…The activation of ferroptosis gives rise to cell death, thus delaying the progression of GC and colorectal cancer (Xu et al 2021 ). The functions of ferroptosis and ferroptosis-associated non-coding RNAs (ncRNAs) in the initiation of GC have attracted much attention recently (Lu et al 2022 ; Wei et al 2021 ). LncRNAs are a diverse class of RNAs that are widely involved in biological processes and perform key roles in chromatin remodeling, transcriptional regulation, and post-transcriptional modification via diverse chromatin-targeted mechanisms and interactions with other RNA species (Dykes and Emanueli 2017 ; Schmitz et al 2016 ).…”

Section: Introductionmentioning

confidence: 99%

POU6F1 promotes ferroptosis by increasing lncRNA-CASC2 transcription to regulate SOCS2/SLC7A11 signaling in gastric cancer

Wang,

Jia,

Jiang

et al. 2024

Cell Biol Toxicol

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Objective This study investigated the effect and mechanism of POU6F1 and lncRNA-CASC2 on ferroptosis of gastric cancer (GC) cells. Methods GC cells treated with erastin and RSL3 were detected for ferroptosis, reactive oxygen species (ROS) level, and cell viability. The expression levels of POU6F1, lncRNA-CASC2, SOCS2, and ferroptosis-related molecules (GPX4 and SLC7A11) were also measured. The regulations among POU6F1, lncRNA-CASC2, FMR1, SOCS2, and SLC7A11 were determined. Subcutaneous tumor models were established, in which the expressions of Ki-67, SOCS2, and GPX4 were detected by immunohistochemistry. Results GC patients with decreased expressions of POU6F1 and lncRNA-CASC2 had lower survival rate. Overexpression of POU6F1 or lncRNA-CASC2 decreased cell proliferation and GSH levels in GC cells, in addition to increasing total iron, Fe2+, MDA, and ROS levels. POU6F1 directly binds to the lncRNA-CASC2 promoter to promote its transcription. LncRNA-CASC2 can target FMR1 and increase SOCS2 mRNA stability to promote SLC7A11 ubiquitination degradation and activate ferroptosis signaling. Knockdown of SOCS2 inhibited the ferroptosis sensitivity of GC cells and reversed the effects of POU6F1 and lncRNA-CASC2 overexpression on ferroptosis in GC cells. Conclusion Transcription factor POU6F1 binds directly to the lncRNA-CASC2 promoter to promote its expression, while upregulated lncRNA-CASC2 increases SOCS2 stability and expression by targeting FMR1, thereby inhibiting SLC7A11 signaling to promote ferroptosis in GC cells and inhibit GC progression.

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Role of ferroptosis and ferroptosis-related non-coding RNAs in the occurrence and development of gastric cancer

Cited by 8 publications

References 53 publications

Helicobacter pylori upregulates circPGD and promotes development of gastric cancer

Helicobacter pylori upregulates circPGD and promotes development of gastric cancer

Ferroptosis and its current progress in gastric cancer

POU6F1 promotes ferroptosis by increasing lncRNA-CASC2 transcription to regulate SOCS2/SLC7A11 signaling in gastric cancer

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