Yijia Sun, Beinan Han, Jiawei Ge, Zijun Huo, Jin Li, Bo Lin, Xin Du, Yimin Zhang, Haiyan Weng, Shuang Yu, Yanbing Li, Haipeng Xiao, Xiaorong Lin, Shubin Hong
{"title":"在甲状腺癌中,CircPSD3通过调节SUCLG2来维持TCA循环和线粒体功能,从而加剧肿瘤进展。","authors":"Yijia Sun, Beinan Han, Jiawei Ge, Zijun Huo, Jin Li, Bo Lin, Xin Du, Yimin Zhang, Haiyan Weng, Shuang Yu, Yanbing Li, Haipeng Xiao, Xiaorong Lin, Shubin Hong","doi":"10.1038/s41419-025-07856-x","DOIUrl":null,"url":null,"abstract":"<p><p>In recent years, there has been a rapid increase in the incidence of thyroid carcinoma (TC). Our study focuses on the regulatory effect of circular RNAs on metabolism of TC, aiming to provide new insights into the mechanisms of progression and a potential therapeutic target for TC. In this study, we identified high expression levels of circPSD3 in TC tissues through RNA sequencing. Papillary thyroid cancer tissue cohorts verified the circPSD3 expression level was positively correlated with larger tumor size. circPSD3 promoted the proliferation of TC cells and reduced apoptosis both in vitro and in vivo. Proteomics and metabolomics suggested that circPSD3 might play a crucial role in regulating the tricarboxylic acid (TCA) cycle. Specifically, circPSD3 acted as a miR-338-5p sponge to upregulate SUCLG2, an enzyme of the TCA cycle, which accelerates the conversion of α-ketoglutarate (α-KG) to succinate. Knockdown of circPSD3 disrupts the TCA cycle and impairs mitochondrial function, resulting in decreased membrane potential and aerobic respiration rate. The reduction in mitochondrial function resulted in the inhibition of proliferation and initiation of mitochondria-mediated apoptosis.</p>","PeriodicalId":9734,"journal":{"name":"Cell Death & Disease","volume":"16 1","pages":"590"},"PeriodicalIF":9.6000,"publicationDate":"2025-09-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12420806/pdf/","citationCount":"0","resultStr":"{\"title\":\"CircPSD3 aggravates tumor progression by maintaining TCA cycle and mitochondrial function via regulating SUCLG2 in thyroid carcinoma.\",\"authors\":\"Yijia Sun, Beinan Han, Jiawei Ge, Zijun Huo, Jin Li, Bo Lin, Xin Du, Yimin Zhang, Haiyan Weng, Shuang Yu, Yanbing Li, Haipeng Xiao, Xiaorong Lin, Shubin Hong\",\"doi\":\"10.1038/s41419-025-07856-x\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>In recent years, there has been a rapid increase in the incidence of thyroid carcinoma (TC). Our study focuses on the regulatory effect of circular RNAs on metabolism of TC, aiming to provide new insights into the mechanisms of progression and a potential therapeutic target for TC. In this study, we identified high expression levels of circPSD3 in TC tissues through RNA sequencing. Papillary thyroid cancer tissue cohorts verified the circPSD3 expression level was positively correlated with larger tumor size. circPSD3 promoted the proliferation of TC cells and reduced apoptosis both in vitro and in vivo. Proteomics and metabolomics suggested that circPSD3 might play a crucial role in regulating the tricarboxylic acid (TCA) cycle. Specifically, circPSD3 acted as a miR-338-5p sponge to upregulate SUCLG2, an enzyme of the TCA cycle, which accelerates the conversion of α-ketoglutarate (α-KG) to succinate. Knockdown of circPSD3 disrupts the TCA cycle and impairs mitochondrial function, resulting in decreased membrane potential and aerobic respiration rate. The reduction in mitochondrial function resulted in the inhibition of proliferation and initiation of mitochondria-mediated apoptosis.</p>\",\"PeriodicalId\":9734,\"journal\":{\"name\":\"Cell Death & Disease\",\"volume\":\"16 1\",\"pages\":\"590\"},\"PeriodicalIF\":9.6000,\"publicationDate\":\"2025-09-09\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12420806/pdf/\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Cell Death & Disease\",\"FirstCategoryId\":\"99\",\"ListUrlMain\":\"https://doi.org/10.1038/s41419-025-07856-x\",\"RegionNum\":1,\"RegionCategory\":\"生物学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q1\",\"JCRName\":\"CELL BIOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Cell Death & Disease","FirstCategoryId":"99","ListUrlMain":"https://doi.org/10.1038/s41419-025-07856-x","RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"CELL BIOLOGY","Score":null,"Total":0}
CircPSD3 aggravates tumor progression by maintaining TCA cycle and mitochondrial function via regulating SUCLG2 in thyroid carcinoma.
In recent years, there has been a rapid increase in the incidence of thyroid carcinoma (TC). Our study focuses on the regulatory effect of circular RNAs on metabolism of TC, aiming to provide new insights into the mechanisms of progression and a potential therapeutic target for TC. In this study, we identified high expression levels of circPSD3 in TC tissues through RNA sequencing. Papillary thyroid cancer tissue cohorts verified the circPSD3 expression level was positively correlated with larger tumor size. circPSD3 promoted the proliferation of TC cells and reduced apoptosis both in vitro and in vivo. Proteomics and metabolomics suggested that circPSD3 might play a crucial role in regulating the tricarboxylic acid (TCA) cycle. Specifically, circPSD3 acted as a miR-338-5p sponge to upregulate SUCLG2, an enzyme of the TCA cycle, which accelerates the conversion of α-ketoglutarate (α-KG) to succinate. Knockdown of circPSD3 disrupts the TCA cycle and impairs mitochondrial function, resulting in decreased membrane potential and aerobic respiration rate. The reduction in mitochondrial function resulted in the inhibition of proliferation and initiation of mitochondria-mediated apoptosis.
期刊介绍:
Brought to readers by the editorial team of Cell Death & Differentiation, Cell Death & Disease is an online peer-reviewed journal specializing in translational cell death research. It covers a wide range of topics in experimental and internal medicine, including cancer, immunity, neuroscience, and now cancer metabolism.
Cell Death & Disease seeks to encompass the breadth of translational implications of cell death, and topics of particular concentration will include, but are not limited to, the following:
Experimental medicine
Cancer
Immunity
Internal medicine
Neuroscience
Cancer metabolism