Article(id=1276976032494260974, tenantId=1146029695717560320, journalId=1276577828834349082, issueId=1276975955985961244, articleNumber=null, orderNo=null, doi=10.19540/j.cnki.cjcmm.20250905.706, pmid=null, cstr=null, oa=null, hot=null, price=null, onlineType=0, articleFormat=0, articleType=null, articleTypeStr=null, receivedDate=1753286400000, receivedDateStr=2025-07-24, revisedDate=null, revisedDateStr=null, acceptedDate=null, acceptedDateStr=null, onlineDate=1782384411214, onlineDateStr=2026-06-25, pubDate=1767196800000, pubDateStr=2026-01-01, doiRegisterDate=null, doiRegisterDateStr=null, onlineIssueDate=1782384411214, onlineIssueDateStr=2026-06-25, onlineJustAcceptDate=null, onlineJustAcceptDateStr=null, onlineFirstDate=null, onlineFirstDateStr=null, sourceXml=null, magXml=null, createTime=1782384411214, creator=13701087609, updateTime=1782384411214, updator=13701087609, issue=Issue{id=1276975955985961244, tenantId=1146029695717560320, journalId=1276577828834349082, year='2026', volume='51', issue='1', pageStart='1', pageEnd='300', issueExtLink='null', onlineDate='null', pubDate='1767196800000', pubDateStr='2026-01-01', beforeIssueId=null, nextIssueId=null, price=null, status=1, issueComplete=1, articleOrder=1, issueType=-1, specialIssue=null, createTime=1782384392973, creator='13701087609', updateTime=1782384484405, updator='13701087609', preIssue=null, nextIssue=null, articleTotal=null, ext={EN=IssueExt(id=1276976339546673871, tenantId=1146029695717560320, journalId=1276577828834349082, issueId=1276975955985961244, language=EN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=), CN=IssueExt(id=1276976339546673872, tenantId=1146029695717560320, journalId=1276577828834349082, issueId=1276975955985961244, language=CN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=)}, issueFiles=null, downloadFileDto=null}, startPage=153, endPage=162, ext={EN=ArticleExt(id=1276976032691393264, articleId=1276976032494260974, tenantId=1146029695717560320, journalId=1276577828834349082, language=EN, title=Transcriptomics and cell experiments reveal regulatory effect of jatrorrhizine on SAT1-mediated ferroptosis in colorectal cancer cell, columnId=null, journalTitle=Chinese Journal of Traditional Chinese Medicine, columnName=null, runingTitle=null, highlight=null, articleAbstract=

This study investigates the inducing effects of jatrorrhizine (JAT), a bioactive compound extracted from Coptidis Rhizoma, on the p53-mediated ferroptosis in human colorectal cancer (CRC) cell lines HT29 and HCT116, specifically through the modulation of spermidine/spermine N1-acetyltransferase 1 (SAT1). Cell viability was assessed via the cell counting kit-8 (CCK-8) assay, while the colony formation assay was employed to determine the proliferative capacity. Cell cycle distribution was analyzed by flow cytometry, and mitochondrial membrane potential was evaluated via JC-1 dye. High-throughput RNA sequencing (RNA-seq) was performed to analyze transcriptomic changes in JAT-treated HT29 and HCT116 cells. Lentiviral transduction was utilized to generate SAT1-overexpressing HCT116 and HT29 cell lines, with transfection efficiency confirmed by qPCR. The levels of intracellular Fe²⁺, reactive oxygen species (ROS), malondialdehyde (MDA), and glutathione (GSH) were quantified via specific commercial assay kits. The protein and mRNA levels of key ferroptosis-related markers: solute carrier family 7 member 11 (SLC7A11), glutathione peroxidase 4 (GPX4), acyl-CoA synthetase long-chain family member 4 (ACSL4), tumor protein p53, and SAT1 were determined by Western blot and qPCR, respectively. The results demonstrated that JAT treatment significantly inhibited both cell viability and proliferation, induced cell cycle arrest, and reduced mitochondrial membrane potential in HCT116 and HT29 cells. RNA-seq results revealed that the KEGG pathways most significantly enriched in JAT-treated cells were protein digestion and absorption, arginine and proline metabolism, glycine, serine and threonine metabolism, and ferroptosis. Notably, the mRNA level of SAT1 in the arginine metabolism pathway was significantly upregulated following JAT treatment. Furthermore, JAT treatment increased the levels of Fe²⁺, ROS, and MDA, while markedly decreasing GSH content in a dose-dependent manner. In addition, the treatment downregulated the protein levels of the ferroptosis inhibitors SLC7A11 and GPX4, and upregulated the expression of the pro-ferroptotic proteins ACSL4, SAT1, and p53. SAT1 overexpression inhibited cell proliferation and activated the p53-mediated ferroptosis signaling pathway. The combination of SAT1 overexpression and JAT treatment (oveSAT1+JAT group) exhibited a synergistic effect, showing superior efficacy over SAT1 overexpression alone (oveSAT1 group). In conclusion, JAT activates the p53-dependent ferroptosis signaling pathway by upregulating the key metabolic enzyme SAT1, which is involved in proline metabolism, thereby inhibiting colorectal cancer cell proliferation.

, authors=null, authorsList=Zhi-yu LI, Song-ling WANG, Wen ZHANG, Xin-yu DAI, Ming-ming ZHOU, Hai-yan PENG, authorCompany=null, correspAuthors=Hai-yan PENG, authorNote=null, correspAuthorsNote=null, copyrightStatement=null, copyrightOwner=null, extLink=null, articleAbsUrl=null, sourceXml=null, magXml=null, pdfUrl=null, pdf=null, pdfFileSize=null, pdfExtLink=null, richHtmlUrl=null, mobilePdfUrl=null, reviewReport=null, pdfFirstPage=null, abstractGraph=null, abstractGraphContent=null, abstractVideo=null, citation=null, cebUrl=null, magXmlContent=null, mapNumber=null, fund=null), CN=ArticleExt(id=1276976032880136946, articleId=1276976032494260974, tenantId=1146029695717560320, journalId=1276577828834349082, language=CN, title=基于转录组学和细胞实验验证探究药根碱对结直肠癌细胞SAT1介导的铁死亡的调控作用, columnId=1276975994707775974, journalTitle=中国中药杂志, columnName=药理, runingTitle=null, highlight=null, articleAbstract=

探讨黄连提取物药根碱（JAT）通过亚精胺／精胺N1-乙酰转移酶1（SAT1）对人结直肠癌（CRC）HT29和HCT116细胞诱导P53介导的铁死亡的影响。采用cell counting kit-8（CCK-8）法检测细胞活力；平板克隆实验检测细胞增殖能力；流式细胞术检测细胞周期；JC-1染料检测线粒体膜电位；用高通量转录组测序（RNA-seq）技术分析JAT处理后HT29和HCT116细胞基因变化。利用慢病毒转染技术构建SAT1过表达HCT116和HT29细胞株，实时荧光定量聚合酶链式反应（real-time qPCR）实验检测转染效率。Fe²⁺、活性氧（ROS）、脂质氧化（MDA）、谷胱甘肽（GSH）检测试剂盒检测CRC细胞株中Fe²⁺、ROS、MDA、GSH表达，蛋白免疫印迹（WB）和qPCR检测胱氨酸／谷氨酸反向转运蛋白（SLC7A11）、谷胱甘肽过氧化物酶4（GPX4）、酰基辅酶A合成酶长链家族成员4（ACSL4）、肿瘤蛋白P53（P53）、SAT1蛋白和mRNA在CRC细胞株中的表达。结果显示，JAT可以抑制HCT116和HT29细胞活力和增殖，诱导细胞周期停滞，降低线粒体膜电位。转录组测序可知JAT对HCT116和HT29细胞主要富集的KEGG通路有蛋白质消化和吸收，精氨酸和脯氨酸代谢，甘氨酸、丝氨酸和苏氨酸代谢，铁死亡等。其中精氨酸代谢途径中的SAT1经JAT处理后mRNA显著上调。且JAT处理后各剂量组在HCT116和HT29细胞中Fe²⁺、ROS、MDA水平升高，GSH含量明显降低，SLC7A11、GPX4蛋白表达降低，ACSL4、SAT1、P53蛋白表达升高。SAT1过表达后的2种CRC细胞株可抑制细胞的增殖，并可激活P53诱导的铁死亡信号通路，而转染SAT1过表达慢病毒（oveSAT1）+JAT组相较于oveSAT1组有更好的效果。综上，JAT可通过上调脯氨酸代谢中SAT1关键分子蛋白激活P53诱导的铁死亡信号通路。

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