Article(id=1292135503512498387, tenantId=1146029695717560320, journalId=1246415772164075586, issueId=1292135444850955150, articleNumber=null, orderNo=null, doi=10.13699/j.cnki.1001-6821.2026.09.017, pmid=null, cstr=null, oa=null, hot=null, price=null, onlineType=0, articleFormat=0, articleType=null, articleTypeStr=null, receivedDate=1768924800000, receivedDateStr=2026-01-21, revisedDate=null, revisedDateStr=null, acceptedDate=null, acceptedDateStr=null, onlineDate=1785998710754, onlineDateStr=2026-08-06, pubDate=1778947200000, pubDateStr=2026-05-17, doiRegisterDate=null, doiRegisterDateStr=null, onlineIssueDate=1785998710754, onlineIssueDateStr=2026-08-06, onlineJustAcceptDate=null, onlineJustAcceptDateStr=null, onlineFirstDate=null, onlineFirstDateStr=null, sourceXml=null, magXml=null, createTime=1785998710754, creator=13701087609, updateTime=1785998710754, updator=13701087609, issue=Issue{id=1292135444850955150, tenantId=1146029695717560320, journalId=1246415772164075586, year='2026', volume='42', issue='9', pageStart='1201', pageEnd='1350', issueExtLink='null', onlineDate='null', pubDate='1778947200000', pubDateStr='2026-05-17', beforeIssueId=null, nextIssueId=null, price=null, status=1, issueComplete=1, articleOrder=1, issueType=-1, specialIssue=null, createTime=1785998696767, creator='13701087609', updateTime=1786014392260, updator='13701087609', preIssue=null, nextIssue=null, articleTotal=null, ext={EN=IssueExt(id=1292201276780081469, tenantId=1146029695717560320, journalId=1246415772164075586, issueId=1292135444850955150, language=EN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=), CN=IssueExt(id=1292201276784275774, tenantId=1146029695717560320, journalId=1246415772164075586, issueId=1292135444850955150, language=CN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=)}, issueFiles=null, downloadFileDto=null}, startPage=1308, endPage=1315, ext={EN=ArticleExt(id=1292135503869014228, articleId=1292135503512498387, tenantId=1146029695717560320, journalId=1246415772164075586, language=EN, title=Research of dihydroartemisinin in promoting ferroptosis by the
miRNA-346/
KLF14 axis-mediated GPX4 signaling pathway to exert anti-tumor effects in cervical cancer, columnId=1246531407326105792, journalTitle=Chinese Journal of Clinical Pharmacology, columnName=Clinical and Basic Bridging Research, runingTitle=null, highlight=null, articleAbstract=
Objective To investigate the effect and mechanism of dihydroartemisinin (DHA) on ferroptosis in cervical cancer by the microRNA (miRNA)-346/Kruppel-like factor 14 (KLF14) axis.
Methods In cell experiment, human cervical cancer Hela cells were treated and divided into several groups including cell normal control group (only HcerEpic cell), cell negative control group (only Hela cell), cell experimental group (Hela cell treated with 246.90 μmol·L-1 DHA for 48 h), DHA+mimic NC group (transferred with mimic NC based on the cell experimental group), DHA+miR-346 mimic group (transfected with miRNA-346 mimic based on the cell experimental group), DHA+sh-NC group (transfected with sh-NC based on the cell experimental group) and DHA+sh-KLF14 group (transfected with sh-KLF14 based on the cell experimental group). In animal experiment, a xenograft tumor model was established by subcutaneous injection of Hela cells into 30 female BALB/c nude mice, which were then divided into the animal control group (gavaged with saline), animal experimental-L group (gavaged with 100 mg·kg-1 DHA) and animal experimental-H group (gavaged with 200 mg·kg-1 DHA), with 10 mice in each group. The relative expression level of miRNA-346 was detected by quantitative real-time polymerase chain reaction. The relative expression levels of KLF14 protein, glutathione peroxidase 4 (GPX4) and solute carrier family 7 member 11 (SLC7A11) were measured by Western blot. Intracellular Fe2+ levels were detected using FerroOrange fluorescent probe. The apoptosis rate was determined by the terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL) assay.
Results In cell experiment, the relative expression levels of miRNA-346 in the cell negative group and cell experimental group were 1.00±0.18 and 0.42±0.06, respectively; the relative expression levels of KLF14 mRNA were 1.00±0.17 and 2.22±0.32, respectively; the relative expression levels of KLF14 protein were 1.00±0.15 and 1.72±0.23, respectively; the relative fluorescence intensities of Fe2+ of cell negative control group, cell experimental group, DHA+mimic NC group, DHA+miRNA-346 mimic group, DHA+sh-NC group and DHA+sh-KLF14 group were 1.00±0.15, 4.86±0.81, 4.32±0.62, 3.12±0.57, 4.23±0.59 and 2.02±0.33, respectively; the relative expression levels of GPX4 protein were 1.00±0.17, 0.45±0.06, 0.48±0.07, 0.78±0.11, 0.44±0.06 and 0.59±0.08, respectively; the relative expression levels of SLC7A11 protein were 1.00±0.12, 0.37±0.05, 0.35±0.04, 0.86±0.12, 0.40±0.07 and 0.77±0.10, respectively; the cell proliferation rates were (100.00±3.65)%, (54.32±7.65)%, (56.32±8.02)%, (72.33±8.65)%, (52.32±9.23)% and (88.25±10.35)%, respectively; the apoptosis rates were (14.32±1.61)%, (61.33±8.25)%, (57.32±7.13)%, (32.44±5.37)%, (59.63±8.98)% and (23.88±3.49)%, respectively. Significant differences were observed in the aforementioned parameters when comparing the cell experimental group with the cell negative group, comparing the DHA + miRNA-346 mimic group with the DHA + mimic NC group, and comparing the DHA + sh-KLF14 group with the DHA + sh-NC group (P<0.01,P<0.001). In animal group, the tumor volumes in the animal control, experimental-L and experimental-H groups were (542.36±92.33), (402.85±92.28) and (295.52±60.56) mm3, respectively; the tumor masses were (1.55±0.33), (1.22±0.22) and(0.88±0.15)g, respectively; the relative positive levels of GPX4 were 1.00±0.18, 0.55±0.07 and 0.42±0.04, respectively; the relative positive levels of SLC7A11 were 1.00±0.16, 0.48±0.06 and 0.29±0.03, respectively. Significant differences were also detected between the animal experimenal-L, -H group and the animal control group (P<0.05, P<0.01, P<0.001).
Conclusion DHA promotes ferroptosis in cervical cancer by the miRNA-346/KLF14 axis-mediated GPX4 signaling pathway.
, authors=Song-jie ZHANG, Li-li ZHANG, Ting LI, Qian-ru LIN, Bin-bin CUI, authorsList=Song-jie ZHANG, Li-li ZHANG, Ting LI, Qian-ru LIN, Bin-bin CUI, authorCompany=null, correspAuthors=Bin-bin CUI, 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=1292135504418468053, articleId=1292135503512498387, tenantId=1146029695717560320, journalId=1246415772164075586, language=CN, title=双氢青蒿素通过
miRNA-346/
KLF14轴介导GPX4信号通路促进宫颈癌铁死亡发挥抗肿瘤作用的研究, columnId=1246531407485489349, journalTitle=中国临床药理学杂志, columnName=临床与基础桥接研究, runingTitle=null, highlight=null, articleAbstract=
目的 研究双氢青蒿素（DHA）通过微小RNA（miRNA）-346/Kruppel样因子14（KLF14）对宫颈癌铁死亡影响及其作用机制。
方法 在细胞实验中，将细胞分为细胞正常对照组（HcerEpic细胞，不予处理）、细胞阴性对照组（Hela细胞，不予处理）、细胞实验组（246.90 μmol·L-1 DHA处理Hela细胞24 h）、DHA+mimic NC组（基于细胞实验组转染mimic NC）、DHA+miRNA-346 mimic组（基于细胞实验组转染miRNA-346 mimic）、DHA+sh-NC组（基于细胞实验组转染sh-NC）和DHA+sh-KLF14组（基于细胞实验组转染sh-KLF14）。在动物实验中，30只雌性BALB/c裸鼠予皮肤注射Hela细胞构建移植瘤模型，随机分为动物对照组（灌胃等量生理盐水）和动物低、高剂量实验组（灌胃100、200 mg·kg-1 DHA），每组10只。用实时荧光定量聚合酶链反应实验法检测miRNA-346相对表达水平；用蛋白印迹法检测KLF14、谷胱甘肽过氧化物酶4（GPX4）和溶质载体家族7成员11（SLC7A11）蛋白相对表达水平；用荧光探针法检测Fe2+水平；用脱氧核糖核苷酸末端转移酶介导的dUTP缺口末端标记法检测细胞凋亡率；用免疫组织化学法检测KLF14和GPX4蛋白水平。
结果 在细胞实验中，细胞阴性对照组和细胞实验组的miRNA-346相对表达水平分别为1.00±0.18和0.42±0.06，KLF14 mRNA相对表达水平分别为1.00±0.17和2.22±0.32，KLF14蛋白相对表达水平分别为1.00±0.15和1.72±0.23；细胞阴性对照组、细胞实验组、DHA+mimic NC组、DHA+miRNA-346 mimic组、DHA+sh-NC组和DHA+sh-KLF14组的Fe2+相对荧光强度分别为1.00±0.15、4.86±0.81、4.32±0.62、3.12±0.57、4.23±0.59和2.02±0.33，GPX4蛋白相对表达水平分别为1.00±0.17、0.45±0.06、0.48±0.07、0.78±0.11、0.44±0.06和0.59±0.08，SLC7A11蛋白相对表达水平分别为1.00±0.12、0.37±0.05、0.35±0.04、0.86±0.12、0.40±0.07和0.77±0.10，细胞增殖率分别为（100.00±3.65）%、（54.32±7.65）%、（56.32±8.02）%、（72.33±8.65）%、（52.32±9.23）%和（88.25±10.35）%，细胞凋亡率分别为（14.32±1.61）%、（61.33±8.25）%、（57.32±7.13）%、（32.44±5.37）%、（59.63±8.98）%和（23.88±3.49）%。细胞实验组与细胞阴性对照组相比，DHA+miRNA-346 mimic组与DHA+mimic NC组相比，DHA+sh-KLF14组与DHA+sh-NC组相比，以上指标在统计学上差异均有统计学意义（P<0.01，P<0.001）。在动物实验中，动物对照组、动物低剂量实验组和动物高剂量实验组的肿瘤体积分别为（542.36±92.33）、（402.85±92.28）和（295.52±60.56）mm3，肿瘤质量分别为（1.55±0.33）、（1.22±0.22）和（0.88±0.15）g，GPX4蛋白相对表达水平分别为1.00±0.18、0.55±0.07和0.42±0.04，SLC7A11蛋白相对表达水平分别为1.00±0.16、0.48±0.06和0.29±0.03。动物低、高剂量实验组与动物对照组相比，以上指标在统计学上差异均有统计学意义（P<0.05，P<0.01，P<0.001）。
结论 DHA可以诱导宫颈癌细胞发生铁积累、抑制GPX4/SLC7A11表达，并促进细胞死亡，提示铁死亡可能参与其抗肿瘤作用，该过程可能与miRNA-346/KLF14轴调控有关。
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张颂婕（1987-），女，副主任医师，主要从事妇科肿瘤与内分泌方面的研究和工作
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