谷胱甘肽过氧化物酶7敲低抑制骨肉瘤细胞的生长、侵袭和迁移，同时增强氧化应激和铁下垂

IF 3.4 2区医学 Q2 Medicine

Journal of Bone Oncology Pub Date : 2025-05-31 DOI:10.1016/j.jbo.2025.100692

Runze He , Xiao Xiao , Xinwen Tang , Chen Lv

{"title":"谷胱甘肽过氧化物酶7敲低抑制骨肉瘤细胞的生长、侵袭和迁移，同时增强氧化应激和铁下垂","authors":"Runze He , Xiao Xiao , Xinwen Tang , Chen Lv","doi":"10.1016/j.jbo.2025.100692","DOIUrl":null,"url":null,"abstract":"<div><h3>Background</h3><div>Glutathione peroxidase 7 (GPX7) possesses antioxidant functions and plays a crucial role in regulating cancer progression. However, relevant evidence in osteosarcoma is scarce. The current study aimed to explore the effect of GPX7 on osteosarcoma progression, oxidative stress, and ferroptosis.</div></div><div><h3>Methods</h3><div>Human osteosarcoma cells (U2OS, MG-63, and SaOS-2) were transfected with GPX7 small interfering RNA (siGPX7). Proliferation, apoptosis, invasion, migration, oxidative stress markers, Fe<sup>2+</sup> levels, and ferroptosis markers were detected in human osteosarcoma cells.</div></div><div><h3>Results</h3><div>GPX7 knockdown inhibited human osteosarcoma cell proliferation, as evidenced by reduced relative cell viability and 5-Ethynyl-2′-deoxyuridine positive cells. GPX7 knockdown also showed a certain ability to promote human osteosarcoma cell apoptosis, as evidenced by increased terminal-deoxynucleotidyl transferase-mediated nick end labeling (TUNEL) positive rate and cleaved-caspase3. GPX7 knockdown decreased invasive and migration rates of human osteosarcoma cells. GPX7 knockdown increased reactive oxygen species and malondialdehyde but decreased mitochondrial membrane potential, suggesting that GPX7 knockdown enhanced oxidative stress in human osteosarcoma cells. Regarding ferroptosis markers, GPX7 knockdown increased acyl-CoA synthetase long-chain family member 4 and reduced solute carrier family 7 member 11; moreover, GPX7 knockdown increased Fe<sup>2+</sup> levels; the above findings indicated that GPX7 knockdown promoted ferroptosis in human osteosarcoma cells.</div></div><div><h3>Conclusion</h3><div>GPX7 knockdown inhibits osteosarcoma cell growth, invasion, and migration while facilitating oxidative stress and ferroptosis.</div></div>","PeriodicalId":48806,"journal":{"name":"Journal of Bone Oncology","volume":"53 ","pages":"Article 100692"},"PeriodicalIF":3.4000,"publicationDate":"2025-05-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Glutathione peroxidase 7 knockdown inhibits growth, invasion, and migration while enhancing oxidative stress and ferroptosis in osteosarcoma cells\",\"authors\":\"Runze He , Xiao Xiao , Xinwen Tang , Chen Lv\",\"doi\":\"10.1016/j.jbo.2025.100692\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<div><h3>Background</h3><div>Glutathione peroxidase 7 (GPX7) possesses antioxidant functions and plays a crucial role in regulating cancer progression. However, relevant evidence in osteosarcoma is scarce. The current study aimed to explore the effect of GPX7 on osteosarcoma progression, oxidative stress, and ferroptosis.</div></div><div><h3>Methods</h3><div>Human osteosarcoma cells (U2OS, MG-63, and SaOS-2) were transfected with GPX7 small interfering RNA (siGPX7). Proliferation, apoptosis, invasion, migration, oxidative stress markers, Fe<sup>2+</sup> levels, and ferroptosis markers were detected in human osteosarcoma cells.</div></div><div><h3>Results</h3><div>GPX7 knockdown inhibited human osteosarcoma cell proliferation, as evidenced by reduced relative cell viability and 5-Ethynyl-2′-deoxyuridine positive cells. GPX7 knockdown also showed a certain ability to promote human osteosarcoma cell apoptosis, as evidenced by increased terminal-deoxynucleotidyl transferase-mediated nick end labeling (TUNEL) positive rate and cleaved-caspase3. GPX7 knockdown decreased invasive and migration rates of human osteosarcoma cells. GPX7 knockdown increased reactive oxygen species and malondialdehyde but decreased mitochondrial membrane potential, suggesting that GPX7 knockdown enhanced oxidative stress in human osteosarcoma cells. Regarding ferroptosis markers, GPX7 knockdown increased acyl-CoA synthetase long-chain family member 4 and reduced solute carrier family 7 member 11; moreover, GPX7 knockdown increased Fe<sup>2+</sup> levels; the above findings indicated that GPX7 knockdown promoted ferroptosis in human osteosarcoma cells.</div></div><div><h3>Conclusion</h3><div>GPX7 knockdown inhibits osteosarcoma cell growth, invasion, and migration while facilitating oxidative stress and ferroptosis.</div></div>\",\"PeriodicalId\":48806,\"journal\":{\"name\":\"Journal of Bone Oncology\",\"volume\":\"53 \",\"pages\":\"Article 100692\"},\"PeriodicalIF\":3.4000,\"publicationDate\":\"2025-05-31\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Journal of Bone Oncology\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://www.sciencedirect.com/science/article/pii/S2212137425000338\",\"RegionNum\":2,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q2\",\"JCRName\":\"Medicine\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of Bone Oncology","FirstCategoryId":"3","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S2212137425000338","RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"Medicine","Score":null,"Total":0}

引用次数: 0

摘要

谷胱甘肽过氧化物酶7 （gtathione peroxidase 7, GPX7）具有抗氧化功能，并在调节癌症进展中发挥重要作用。然而，骨肉瘤的相关证据很少。本研究旨在探讨GPX7对骨肉瘤进展、氧化应激和铁下垂的影响。方法用GPX7小干扰RNA （siGPX7）转染人骨肉瘤细胞（U2OS、MG-63、SaOS-2）。检测了人骨肉瘤细胞的增殖、凋亡、侵袭、迁移、氧化应激标志物、Fe2+水平和铁下垂标志物。结果gpx7基因敲低可抑制人骨肉瘤细胞的增殖，降低细胞的相对活力和5-乙基-2 ' -脱氧尿苷阳性细胞。GPX7敲低也显示出一定的促进人骨肉瘤细胞凋亡的能力，这可以通过增加终端脱氧核苷酸转移酶介导的nick end labeling （TUNEL）阳性率和cleaved-caspase3来证明。GPX7敲低可降低人骨肉瘤细胞的侵袭和迁移率。GPX7敲低增加了活性氧和丙二醛，但降低了线粒体膜电位，表明GPX7敲低增强了人骨肉瘤细胞的氧化应激。在铁下垂标志物方面，GPX7敲低增加了酰基辅酶a合成酶长链家族成员4，降低了溶质载体家族7成员11；GPX7敲低使Fe2+水平升高；上述结果表明，敲低GPX7可促进人骨肉瘤细胞铁下垂。结论px7基因敲低抑制骨肉瘤细胞生长、侵袭和迁移，促进氧化应激和铁下垂。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

Glutathione peroxidase 7 knockdown inhibits growth, invasion, and migration while enhancing oxidative stress and ferroptosis in osteosarcoma cells

查看原文本刊更多论文

Glutathione peroxidase 7 knockdown inhibits growth, invasion, and migration while enhancing oxidative stress and ferroptosis in osteosarcoma cells

Background

Glutathione peroxidase 7 (GPX7) possesses antioxidant functions and plays a crucial role in regulating cancer progression. However, relevant evidence in osteosarcoma is scarce. The current study aimed to explore the effect of GPX7 on osteosarcoma progression, oxidative stress, and ferroptosis.

Methods

Human osteosarcoma cells (U2OS, MG-63, and SaOS-2) were transfected with GPX7 small interfering RNA (siGPX7). Proliferation, apoptosis, invasion, migration, oxidative stress markers, Fe²⁺ levels, and ferroptosis markers were detected in human osteosarcoma cells.

Results

GPX7 knockdown inhibited human osteosarcoma cell proliferation, as evidenced by reduced relative cell viability and 5-Ethynyl-2′-deoxyuridine positive cells. GPX7 knockdown also showed a certain ability to promote human osteosarcoma cell apoptosis, as evidenced by increased terminal-deoxynucleotidyl transferase-mediated nick end labeling (TUNEL) positive rate and cleaved-caspase3. GPX7 knockdown decreased invasive and migration rates of human osteosarcoma cells. GPX7 knockdown increased reactive oxygen species and malondialdehyde but decreased mitochondrial membrane potential, suggesting that GPX7 knockdown enhanced oxidative stress in human osteosarcoma cells. Regarding ferroptosis markers, GPX7 knockdown increased acyl-CoA synthetase long-chain family member 4 and reduced solute carrier family 7 member 11; moreover, GPX7 knockdown increased Fe²⁺ levels; the above findings indicated that GPX7 knockdown promoted ferroptosis in human osteosarcoma cells.

Conclusion

GPX7 knockdown inhibits osteosarcoma cell growth, invasion, and migration while facilitating oxidative stress and ferroptosis.

求助全文

通过发布文献求助，成功后即可免费获取论文全文。去求助

来源期刊

Journal of Bone Oncology ONCOLOGY-

CiteScore

7.20

自引率

2.90%

发文量

审稿时长

34 days

期刊介绍： The Journal of Bone Oncology is a peer-reviewed international journal aimed at presenting basic, translational and clinical high-quality research related to bone and cancer. As the first journal dedicated to cancer induced bone diseases, JBO welcomes original research articles, review articles, editorials and opinion pieces. Case reports will only be considered in exceptional circumstances and only when accompanied by a comprehensive review of the subject. The areas covered by the journal include: Bone metastases (pathophysiology, epidemiology, diagnostics, clinical features, prevention, treatment) Preclinical models of metastasis Bone microenvironment in cancer (stem cell, bone cell and cancer interactions) Bone targeted therapy (pharmacology, therapeutic targets, drug development, clinical trials, side-effects, outcome research, health economics) Cancer treatment induced bone loss (epidemiology, pathophysiology, prevention and management) Bone imaging (clinical and animal, skeletal interventional radiology) Bone biomarkers (clinical and translational applications) Radiotherapy and radio-isotopes Skeletal complications Bone pain (mechanisms and management) Orthopaedic cancer surgery Primary bone tumours Clinical guidelines Multidisciplinary care Keywords: bisphosphonate, bone, breast cancer, cancer, CTIBL, denosumab, metastasis, myeloma, osteoblast, osteoclast, osteooncology, osteo-oncology, prostate cancer, skeleton, tumour.