STC2 activates PRMT5 to induce radioresistance through DNA damage repair and ferroptosis pathways in esophageal squamous cell carcinoma

Jiang, Kan; Yin, Xin; Zhang, Qingyi; Yin, Jie; Tang, Qiuying; Xu, Mengyou; Wu, Lingyun; Shen, Yifan; Zhou, Ziyang; Yu, Hao; Yan, Senxiang

doi:10.1016/j.redox.2023.102626

Cited by 24 publications

(17 citation statements)

References 63 publications

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Section: Discussionmentioning

confidence: 99%

“…The mechanism of radioresistance in GBM have been identified regulated by various cellular signalling mechanisms, including DDR, cell cycle regulation, 7 , 8 and cell apoptosis. 9 , 10 However, effective radiosensitizer that can increase the efficacy of RT have not yet been developed. In the current research, we identified a RT related DEG—GSN by combining examination of RNA sequencing and bioinformatics analysis of GBM.…”

Section: Discussionmentioning

confidence: 99%

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Gelsolin knockdown confers radiosensitivity to glioblastoma cells

Gao,

Jiang,

Liu

2024

Cancer Medicine

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ObjectiveRadiotherapy (RT) is a cornerstone of the glioblastoma (GBM) treatment. However, the resistance of tumour cells to radiation results in early recurrence. The mechanisms underlying GBM radioresistance remain unclear. Screening for differentially expressed genes (DEGs) related to radiation might be a potential solution to this problem.MethodRT‐associated DEGs were screened based on the RNA sequencing of 15 paired primary and recurrent GBMs. The mRNA and protein expression of candidate genes were validated in RNA sequencing of The Chinese Genome Atlas (CGGA) dataset and 18 cases of GBM samples. The relationship between the candidate gene and radiation was confirmed in irradiated GBM cells. The association of candidate gene with clinical characteristics and survival was investigated in the CGGA and TCGA dataset. Biological function and pathway analysis were explored by gene ontology analysis. The association of the candidate gene with radiosensitivity was verified using cell counting Kit‐8, comet, and colony formation assays in vitro and subcutaneous tumour xenograft experiments in vivo.ResultsGelsolin (GSN) was selected for further study. GSN expression was significant elevated in recurrent GBM and up‐regulated in irradiated GBM cell lines. High expression of GSN was enriched in malignant phenotype of glioma. Moreover, high expression of GSN was associated with poor prognosis. Further investigation demonstrated that GSN‐knockdown (GSN‐KD) combined with RT significantly inhibited cell proliferation and enhanced radiosensitivity in vivo and in vitro. Mechanistically, GSN‐KD could lead to more serious DNA damage and promotes apoptosis after RT.ConclusionRadiation induced up‐regulated of GSN. GSN‐KD could enhance the radiosensitivity of GBM.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Gelsolin knockdown confers radiosensitivity to glioblastoma cells

Gao,

Jiang,

Liu

2024

Cancer Medicine

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“…Su et al identified BTB domain and CNC homology 1 (BACH1) as a cellular factor that strongly interacts with P53 R175H [ 252 ], and p53 R175H acts as a repressor for ferroptosis by abrogating BACH1-mediated downregulation of SLC7A11 to enhance tumor growth [ 252 ]. In addition, Chang et al revealed that STC2 could interact with protein methyltransferase 5 (PRMT5) and activate PRMT5 to participate in SLC7A11 mediated ferroptosis [ 259 ]. Ovarian cancer (OC) is the seventh most common malignant tumor and ranks eighth among the causes of cancer death in females [ 301 ].…”

Section: Ferroptosis In Pathologiesmentioning

confidence: 99%

The mechanism of ferroptosis and its related diseases

Feng,

Tang,

Wang

et al. 2023

Mol Biomed

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Ferroptosis, a regulated form of cellular death characterized by the iron-mediated accumulation of lipid peroxides, provides a novel avenue for delving into the intersection of cellular metabolism, oxidative stress, and disease pathology. We have witnessed a mounting fascination with ferroptosis, attributed to its pivotal roles across diverse physiological and pathological conditions including developmental processes, metabolic dynamics, oncogenic pathways, neurodegenerative cascades, and traumatic tissue injuries. By unraveling the intricate underpinnings of the molecular machinery, pivotal contributors, intricate signaling conduits, and regulatory networks governing ferroptosis, researchers aim to bridge the gap between the intricacies of this unique mode of cellular death and its multifaceted implications for health and disease. In light of the rapidly advancing landscape of ferroptosis research, we present a comprehensive review aiming at the extensive implications of ferroptosis in the origins and progress of human diseases. This review concludes with a careful analysis of potential treatment approaches carefully designed to either inhibit or promote ferroptosis. Additionally, we have succinctly summarized the potential therapeutic targets and compounds that hold promise in targeting ferroptosis within various diseases. This pivotal facet underscores the burgeoning possibilities for manipulating ferroptosis as a therapeutic strategy. In summary, this review enriched the insights of both investigators and practitioners, while fostering an elevated comprehension of ferroptosis and its latent translational utilities. By revealing the basic processes and investigating treatment possibilities, this review provides a crucial resource for scientists and medical practitioners, aiding in a deep understanding of ferroptosis and its effects in various disease situations.

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“…In terms of mechanism, low expression of COMMD10 inhibited hypoxia‐inducible factor‐1 alpha (HIF‐1α) degradation and promoted HIF‐1α nuclear translocation by enhancing Cu accumulation, which suppressed ferroptosis in HCC cells by facilitating the expression of SLC7A11 and ceruloplasmin. Analogously, stanniocalcin 2 (STC2)‐mediated overexpression of SLC7A11 contributed to radioresistance in ESCC (K. Jiang, Yin, et al, 2023). Chen et al revealed that the suppressor of cytokine signaling 2 (SOCS2) was underexpressed in radioresistant HCC tissues and that SOCS2 overexpression enhanced the sensitivity of HCC cells to ferroptosis and radiation via increasing the polyubiquitination and degradation of SLC7A11 (Q. Chen, Zheng, et al, 2023).…”

Section: Multifaceted Roles Of Ferroptosis In Cancermentioning

confidence: 99%

Ferroptosis: Potential opportunities for natural products in cancer therapy

Nie,

Shen,

Zhou

et al. 2023

Phytotherapy Research

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Cancer cells often exhibit defects in the execution of cell death, resulting in poor clinical outcomes for patients with many cancer types. Ferroptosis is a newly discovered form of programmed cell death characterized by intracellular iron overload and lipid peroxidation in the cell membrane. Increasing evidence suggests that ferroptosis is closely associated with a wide variety of physiological and pathological processes, particularly in cancer. Notably, various bioactive natural products have been shown to induce the initiation and execution of ferroptosis in cancer cells, thereby exerting anticancer effects. In this review, we summarize the core regulatory mechanisms of ferroptosis and the multifaceted roles of ferroptosis in cancer. Importantly, we focus on natural products that regulate ferroptosis in cancer cells, such as terpenoids, polyphenols, alkaloids, steroids, quinones, and polysaccharides. The clinical efficacy, adverse effects, and drug–drug interactions of these natural products need to be evaluated in further high‐quality studies to accelerate their application in cancer treatment.

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STC2 activates PRMT5 to induce radioresistance through DNA damage repair and ferroptosis pathways in esophageal squamous cell carcinoma

Cited by 24 publications

References 63 publications

Gelsolin knockdown confers radiosensitivity to glioblastoma cells

Gelsolin knockdown confers radiosensitivity to glioblastoma cells

The mechanism of ferroptosis and its related diseases

Ferroptosis: Potential opportunities for natural products in cancer therapy

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