<scp><i>CircRPPH1</i></scp> promotes the stemness of gastric cancer cells by targeting <i><scp>miR</scp>‐375/<scp>SLC7A11</scp></i> axis

Liu, Jiayun; Yang, Huanjuan; Deng, Jie; Jiang, Rongqi; Meng, Enqing; Wu, Hao

doi:10.1002/tox.23668

Cited by 15 publications

(7 citation statements)

References 33 publications

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“…Existing study has confirmed that GC patients with unbalanced expression of SLC7A11-AS1/xCT axis had a poor prognosis and relatively poor response to chemotherapy [ 19 ]. SLC7A11 also acts as an epigenetic co-factor to interfere with the stemness of GC cells [ 20 ]. RAC1 (Ras-related C3 botulinum toxin substrate 1) is a small GTPase, the upregulation of which activates disulfidptosis [ 6 ].…”

Section: Discussionmentioning

confidence: 99%

Unravelling diagnostic clusters and immune landscapes of disulfidptosis patterns in gastric cancer through bioinformatic assay

Zhang,

Chen,

Lin

et al. 2023

Aging

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Disulfidptosis is a novel type of cell death mediated by SLC7A11-induced disulfide stress. Gastric cancer (GC) is a common malignant gastrointestinal tumor. Existing evidence shows that SLC7A11 can regulate cell death and improve the progression of GC, suggesting disulfidptosis may exist in the pathological process of GC. However, the underlying functions of disulfidptosis regulators in GC remain unknown. The dataset of GSE54129 was screened to comprehensively investigate the disulfidptosis-related diagnostic clusters and immune landscapes in GC. Totally 15 significant disulfidptosis regulators were identified via difference analysis between GC samples and controls. Then random forest model was utilized to assess their importance score (mean decrease Gini). Then a nomogram model was constructed, which could offer benefit to patients based on our subsequent decision curve analysis. All the included GC patients were divided into 2 disulfidptosis subgroups (clusterA and clusterB) according to the significant disulfidptosis regulators in virtue of consensus clustering analysis. The disulfidptosis score of each sample was calculated through PCA algorithms to quantify the disulfidptosis subtypes. Patients from clusterB exhibited lower disulfidptosis scores than those of patients in clusterA. In addition, we found that the cases in clusterB were closely associated with the immunity of activated CD4 T cell, etc., while clusterA was linked to immature dendritic cell, mast cell, natural killer T cell, natural killer cell, etc., which has a higher disulfidptosis score. Therefore, disulfidptosis regulators play an important role in the pathological process of GC, providing a promising marker and an immunotherapeutic strategy for future GC therapy.

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Section: Discussionmentioning

confidence: 99%

Unravelling diagnostic clusters and immune landscapes of disulfidptosis patterns in gastric cancer through bioinformatic assay

Zhang,

Chen,

Lin

et al. 2023

Aging

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“…Recent research has revealed that in GC cells, miR-375 can directly interact with circRPPH1. The latter is highly expressed in GC cells and relies on the miR-375/SLC7A11 axis to enhance the stemness of GC cells ( Liu et al, 2023 ). Gao et al found that circ0008035 acts as a sponge for miR-302a, thereby increasing the expression of downstream protein target E2F7 in GC cells.…”

Section: The Regulatory Mechanisms Of Ferroptosis In Gc Cellsmentioning

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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“…SLC7A11 and GPX4, two important ferroptosis suppressors and markers, are targets not only for small molecules as ferroptosis inducers but also for a large group of ncRNAs regulating ferroptosis. MiR-409-3p, miR-515-5p, miR-375, miR-1261, miR-489-3p, miR-128-3p, miR-545-3p, miR-5096, miR-520d-5p, miR-125b-5p, miR-34c-3p, miR-143-3p, miR-26a-5p, miR-27b-3p, miR-587, miR-194-5p, miR-27a-3p, miR-520a-5p, miR-1184, miR-6077, miR-485-5p, miR-25-3p, miR-513a-3p, miR-206, and miR-431 have been reported to target and repress SLC7A11 to promote ferroptosis in cervical cancer [233], gastric cancer [148,234,235], liver cancer [236], prostate cancer [146], thyroid cancer [237], breast cancer [238], oral squamous cell carcinoma [239][240][241], kidney cancer [242,243], ovarian cancer [244,245], lung cancer [147,[246][247][248][249], prostate cancer [250], esophageal squamous cell carcinoma [251], osteosarcoma [252], and colorectal cancer [253]. MiR-378a-3p, miR-27a, miR-144-3p, and exosomal miR-26b-5p from patients with acute myocardial infarction target and reduce SLC7A11 expression to induce ferroptosis in the IRI of the kidney [254], brain [255], and heart [256,257].…”

Section: Ncrnas Regulating Ferroptosis Through Antioxidant Defensementioning

confidence: 99%

The Regulation of Ferroptosis by Noncoding RNAs

Zheng,

Zhang

2023

IJMS

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As a novel form of regulated cell death, ferroptosis is characterized by intracellular iron and lipid peroxide accumulation, which is different from other regulated cell death forms morphologically, biochemically, and immunologically. Ferroptosis is regulated by iron metabolism, lipid metabolism, and antioxidant defense systems as well as various transcription factors and related signal pathways. Emerging evidence has highlighted that ferroptosis is associated with many physiological and pathological processes, including cancer, neurodegeneration diseases, cardiovascular diseases, and ischemia/reperfusion injury. Noncoding RNAs are a group of functional RNA molecules that are not translated into proteins, which can regulate gene expression in various manners. An increasing number of studies have shown that noncoding RNAs, especially miRNAs, lncRNAs, and circRNAs, can interfere with the progression of ferroptosis by modulating ferroptosis-related genes or proteins directly or indirectly. In this review, we summarize the basic mechanisms and regulations of ferroptosis and focus on the recent studies on the mechanism for different types of ncRNAs to regulate ferroptosis in different physiological and pathological conditions, which will deepen our understanding of ferroptosis regulation by noncoding RNAs and provide new insights into employing noncoding RNAs in ferroptosis-associated therapeutic strategies.

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CircRPPH1 promotes the stemness of gastric cancer cells by targeting miR‐375/SLC7A11 axis

Cited by 15 publications

References 33 publications

Unravelling diagnostic clusters and immune landscapes of disulfidptosis patterns in gastric cancer through bioinformatic assay

Unravelling diagnostic clusters and immune landscapes of disulfidptosis patterns in gastric cancer through bioinformatic assay

Ferroptosis and its current progress in gastric cancer

The Regulation of Ferroptosis by Noncoding RNAs

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