Article(id=1321501041280004975, tenantId=1146029695717560320, journalId=1246415837536497731, issueId=1321500868936052946, articleNumber=PA20260310_viV2u8cO, orderNo=null, doi=10.12307/2026.540, pmid=null, cstr=null, oa=null, hot=null, price=null, onlineType=0, articleFormat=0, articleType=null, articleTypeStr=null, receivedDate=null, receivedDateStr=null, revisedDate=null, revisedDateStr=null, acceptedDate=1743609600000, acceptedDateStr=2025-04-03, onlineDate=1748534400000, onlineDateStr=2025-05-30, pubDate=1767801600000, pubDateStr=2026-01-08, doiRegisterDate=null, doiRegisterDateStr=null, onlineIssueDate=1793000000542, onlineIssueDateStr=2026-10-26, onlineJustAcceptDate=null, onlineJustAcceptDateStr=null, onlineFirstDate=null, onlineFirstDateStr=null, sourceXml=null, magXml=null, createTime=1793000000542, creator=admin, updateTime=1793000000542, updator=admin, issue=Issue{id=1321500868936052946, tenantId=1146029695717560320, journalId=1246415837536497731, year='2026', volume='30', issue='1', pageStart='null', pageEnd='null', issueExtLink='null', onlineDate='null', pubDate='1767801600000', pubDateStr='2026-01-08', beforeIssueId=null, nextIssueId=null, price=null, status=1, issueComplete=0, articleOrder=1, issueType=-1, specialIssue=null, createTime=1792999959453, creator='ztmeta', updateTime=1792999959453, updator='ztmeta', preIssue=null, nextIssue=null, articleTotal=null, ext=null, issueFiles=null, downloadFileDto=null}, startPage=130, endPage=138, ext={EN=ArticleExt(id=1321501044832580465, articleId=1321501041280004975, tenantId=1146029695717560320, journalId=1246415837536497731, language=EN, title=Choline kinase alpha silencing affects proliferation and apoptosis in glioma cells by inducing mitochondrial dysfunction, columnId=null, journalTitle=Chinese Journal of Tissue Engineering Research, columnName=工程化细胞及干细胞培养与分化, runingTitle=null, highlight=null, articleAbstract=BACKGROUND: Choline kinase alpha is a key enzyme in phospholipid metabolism, involved in the synthesis of phosphatidylcholine, and plays an important role in maintaining cell membrane integrity and signal transduction. Research has shown that choline kinase alpha is highly expressed in various tumors and is closely related to cell proliferation, metabolic reprogramming, and tumor progression. As a potential therapeutic target, the role of choline kinase alpha in tumor metabolism and mitochondrial function still needs further exploration. OBJECTIVE: To evaluate the effects and the underlying mechanisms of choline kinase alpha on the proliferation and apoptosis of glioma U87MG and U251 cells. METHODS: Short hairpin RNA of choline kinase alpha and its empty vector control were transfected into U87MG and U251 glioma cells. Mitochondrial morphology was observed by transmission electron microscopy. Mitochondrial structure and functional protein levels were assessed by western blot assay. Reactive oxygen species levels in cells were measured using a reactive oxygen species fluorescent probe. Mitochondrial membrane potential was assessed with a JC-1 assay. Intracellular adenosine triphosphate levels were measured by chemiluminescence. Cell proliferation was evaluated using a CCK-8 assay. Apoptosis levels were analyzed by flow cytometry. The mitochondrial fission inhibitor Mdivi-1 was used to protect the mitochondrial function of the choline kinase α-silenced lentiviral cells. Finally, U87MG cells were subcutaneously injected to construct a subcutaneous tumor model in nude mice. The tumor growth in nude mice was observed before and after choline kinase alpha silencing and after the use of the mitochondrial fission inhibitor Mdivi-1. RESULTS AND CONCLUSION: (1) Compared with the empty control group, the mitochondria of U87MG and U251 cells in the choline kinase alpha silencing lentivirus group exhibited significant structural abnormalities in mitochondria, such as vacuolization and cristae disruption. The expressions of mitochondrial structure and function-related proteins TOM20, ACO2, and ATP5A were significantly decreased (P < 0.01, P < 0.001), the expression of SOD2 was significantly increased (P < 0.01, P < 0.000 1), the fluorescence intensity of reactive oxygen species was significantly increased (P < 0.01), the mitochondrial membrane potential and adenosine triphosphate level were significantly decreased (P < 0.01, P < 0.001), the cell proliferation ability was reduced (P < 0.01), and the apoptosis level was increased (P < 0.001). (2) Following Mdivi-1 treatment, the fluorescence intensity of reactive oxygen species in U87MG and U251 cells decreased (P < 0.05, P < 0.01), mitochondrial membrane potential and adenosine triphosphate levels were significantly restored (P < 0.05, P < 0.01, P < 0.001), cell proliferation ability was improved (P < 0.05, P < 0.01), and apoptosis level was decreased (P < 0.05). (3) In addition, the in vitro subcutaneous tumor formation experiment of nude mice showed that compared with the empty control group, the mass and growth rate of subcutaneous tumors formed by U87MG cells in the choline kinase alpha silencing lentivirus group were significantly reduced (P < 0.000 1). After Mdivi-1 treatment, the mass and growth rate of tumors were significantly increased (P < 0.000 1). (4) The results show that choline kinase alpha silencing affects the proliferation and apoptosis of glioma cells by inducing mitochondrial dysfunction., authors=null, authorsList=null, authorCompany=null, correspAuthors=null, 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=1321501044744500080, articleId=1321501041280004975, tenantId=1146029695717560320, journalId=1246415837536497731, language=CN, title=胆碱激酶α沉默诱导线粒体功能障碍影响胶质瘤细胞的增殖和凋亡, columnId=null, journalTitle=中国组织工程研究, columnName=工程化细胞及干细胞培养与分化, runingTitle=null, highlight=null, articleAbstract=背景:胆碱激酶α是磷脂代谢的关键酶,参与磷脂酰胆碱的合成,在维持细胞膜完整性和信号传导中起重要作用。研究表明,胆碱激酶α在多种肿瘤中高表达,与细胞增殖、代谢重编程和肿瘤进展密切相关。作为潜在的治疗靶点,胆碱激酶α在肿瘤代谢和线粒体功能中的作用尚需进一步探讨。 目的:评估胆碱激酶α对胶质瘤U87MG和U251细胞增殖和凋亡的影响及机制。 方法:将胆碱激酶α沉默慢病毒及空载对照病毒转染至胶质瘤U87MG和U251细胞中,通过透射电镜观察线粒体形态,利用Western blot检测线粒体结构和功能蛋白的表达,活性氧荧光探针检测细胞内的活性氧水平,JC-1试剂盒检测线粒体膜电位,化学发光法测定细胞内ATP含量,CCK-8检测细胞增殖能力,流式细胞术检测细胞凋亡水平;然后采用线粒体分裂抑制剂Mdivi-1保护胆碱激酶α沉默慢病毒细胞的线粒体功能。最后皮下注射U87MG细胞构建裸鼠皮下肿瘤模型,观察胆碱激酶α沉默前后以及使用线粒体分裂抑制剂Mdivi-1后裸鼠肿瘤生长情况。 结果与结论:①与空载对照组细胞相比,胆碱激酶α沉默慢病毒组U87MG和U251细胞的线粒体出现明显空泡化和线粒体嵴断裂等结构异常现象,线粒体结构和功能相关蛋白TOM20、ACO2和ATP5A表达均显著下降(P < 0.01,P < 0.001),SOD2表达显著上升(P < 0.01,P < 0.000 1),活性氧荧光强度显著增加(P < 0.01),线粒体膜电位和ATP水平显著降低(P < 0.01,P < 0.001),细胞增殖能力降低(P < 0.01),凋亡水平提高(P < 0.001);②加入Mdivi-1处理后,U87MG和U251细胞的活性氧荧光强度降低(P < 0.05,P < 0.01),线粒体膜电位和ATP水平均显著恢复(P < 0.05,P < 0.01,P < 0.001),细胞增殖能力提高(P < 0.05,P < 0.01),凋亡水平下降(P < 0.05);③此外,体外裸鼠皮下成瘤实验显示,与空载对照组相比,胆碱激酶α沉默慢病毒组U87MG细胞形成的皮下肿瘤质量和生长速度显著降低(P < 0.000 1),Mdivi-1处理后,肿瘤质量和生长速度显著增加(P < 0.000 1);④结果表明,胆碱激酶α沉默诱导线粒体功能障碍影响胶质瘤细胞的增殖和凋亡。, authors=null, authorsList=null, authorCompany=null, correspAuthors=null, authorNote=null, correspAuthorsNote=null, copyrightStatement=null, copyrightOwner=null, extLink=null, articleAbsUrl=null, sourceXml=null, magXml=null, 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胆碱激酶α沉默诱导线粒体功能障碍影响胶质瘤细胞的增殖和凋亡
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赵阳 1 , 李嘉麟 2 , 吴箫 1 , 邹有瑞 3, , 刘阳 3, , 马辉 3,
中国组织工程研究 | 工程化细胞及干细胞培养与分化 2026,30(1): 130-138
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中国组织工程研究 |工程化细胞及干细胞培养与分化 2026 , 30 (1) : 130 -138
胆碱激酶α沉默诱导线粒体功能障碍影响胶质瘤细胞的增殖和凋亡
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赵阳1 , 李嘉麟2, 吴箫1, 邹有瑞3,, 刘阳3,, 马辉3,
作者信息
  • 1.夏医科大学,宁夏回族自治区银川市 750004
  • 2.津市天津医院,天津市 300000
  • 3.夏医科大学总医院,宁夏回族自治区银川市 750004
  • 4.夏医科大学总医院,宁夏回族自治区银川市 750004
Choline kinase alpha silencing affects proliferation and apoptosis in glioma cells by inducing mitochondrial dysfunction
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出版时间: 2026-01-08 doi: 10.12307/2026.540
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背景:胆碱激酶α是磷脂代谢的关键酶,参与磷脂酰胆碱的合成,在维持细胞膜完整性和信号传导中起重要作用。研究表明,胆碱激酶α在多种肿瘤中高表达,与细胞增殖、代谢重编程和肿瘤进展密切相关。作为潜在的治疗靶点,胆碱激酶α在肿瘤代谢和线粒体功能中的作用尚需进一步探讨。 目的:评估胆碱激酶α对胶质瘤U87MG和U251细胞增殖和凋亡的影响及机制。 方法:将胆碱激酶α沉默慢病毒及空载对照病毒转染至胶质瘤U87MG和U251细胞中,通过透射电镜观察线粒体形态,利用Western blot检测线粒体结构和功能蛋白的表达,活性氧荧光探针检测细胞内的活性氧水平,JC-1试剂盒检测线粒体膜电位,化学发光法测定细胞内ATP含量,CCK-8检测细胞增殖能力,流式细胞术检测细胞凋亡水平;然后采用线粒体分裂抑制剂Mdivi-1保护胆碱激酶α沉默慢病毒细胞的线粒体功能。最后皮下注射U87MG细胞构建裸鼠皮下肿瘤模型,观察胆碱激酶α沉默前后以及使用线粒体分裂抑制剂Mdivi-1后裸鼠肿瘤生长情况。 结果与结论:①与空载对照组细胞相比,胆碱激酶α沉默慢病毒组U87MG和U251细胞的线粒体出现明显空泡化和线粒体嵴断裂等结构异常现象,线粒体结构和功能相关蛋白TOM20、ACO2和ATP5A表达均显著下降(P < 0.01,P < 0.001),SOD2表达显著上升(P < 0.01,P < 0.000 1),活性氧荧光强度显著增加(P < 0.01),线粒体膜电位和ATP水平显著降低(P < 0.01,P < 0.001),细胞增殖能力降低(P < 0.01),凋亡水平提高(P < 0.001);②加入Mdivi-1处理后,U87MG和U251细胞的活性氧荧光强度降低(P < 0.05,P < 0.01),线粒体膜电位和ATP水平均显著恢复(P < 0.05,P < 0.01,P < 0.001),细胞增殖能力提高(P < 0.05,P < 0.01),凋亡水平下降(P < 0.05);③此外,体外裸鼠皮下成瘤实验显示,与空载对照组相比,胆碱激酶α沉默慢病毒组U87MG细胞形成的皮下肿瘤质量和生长速度显著降低(P < 0.000 1),Mdivi-1处理后,肿瘤质量和生长速度显著增加(P < 0.000 1);④结果表明,胆碱激酶α沉默诱导线粒体功能障碍影响胶质瘤细胞的增殖和凋亡。
胆碱激酶α  /  胶质母细胞瘤  /  线粒体功能  /  Mdivi-1  /  活性氧  /  线粒体膜电位  /  增殖  /  凋亡
BACKGROUND: Choline kinase alpha is a key enzyme in phospholipid metabolism, involved in the synthesis of phosphatidylcholine, and plays an important role in maintaining cell membrane integrity and signal transduction. Research has shown that choline kinase alpha is highly expressed in various tumors and is closely related to cell proliferation, metabolic reprogramming, and tumor progression. As a potential therapeutic target, the role of choline kinase alpha in tumor metabolism and mitochondrial function still needs further exploration. OBJECTIVE: To evaluate the effects and the underlying mechanisms of choline kinase alpha on the proliferation and apoptosis of glioma U87MG and U251 cells. METHODS: Short hairpin RNA of choline kinase alpha and its empty vector control were transfected into U87MG and U251 glioma cells. Mitochondrial morphology was observed by transmission electron microscopy. Mitochondrial structure and functional protein levels were assessed by western blot assay. Reactive oxygen species levels in cells were measured using a reactive oxygen species fluorescent probe. Mitochondrial membrane potential was assessed with a JC-1 assay. Intracellular adenosine triphosphate levels were measured by chemiluminescence. Cell proliferation was evaluated using a CCK-8 assay. Apoptosis levels were analyzed by flow cytometry. The mitochondrial fission inhibitor Mdivi-1 was used to protect the mitochondrial function of the choline kinase α-silenced lentiviral cells. Finally, U87MG cells were subcutaneously injected to construct a subcutaneous tumor model in nude mice. The tumor growth in nude mice was observed before and after choline kinase alpha silencing and after the use of the mitochondrial fission inhibitor Mdivi-1. RESULTS AND CONCLUSION: (1) Compared with the empty control group, the mitochondria of U87MG and U251 cells in the choline kinase alpha silencing lentivirus group exhibited significant structural abnormalities in mitochondria, such as vacuolization and cristae disruption. The expressions of mitochondrial structure and function-related proteins TOM20, ACO2, and ATP5A were significantly decreased (P < 0.01, P < 0.001), the expression of SOD2 was significantly increased (P < 0.01, P < 0.000 1), the fluorescence intensity of reactive oxygen species was significantly increased (P < 0.01), the mitochondrial membrane potential and adenosine triphosphate level were significantly decreased (P < 0.01, P < 0.001), the cell proliferation ability was reduced (P < 0.01), and the apoptosis level was increased (P < 0.001). (2) Following Mdivi-1 treatment, the fluorescence intensity of reactive oxygen species in U87MG and U251 cells decreased (P < 0.05, P < 0.01), mitochondrial membrane potential and adenosine triphosphate levels were significantly restored (P < 0.05, P < 0.01, P < 0.001), cell proliferation ability was improved (P < 0.05, P < 0.01), and apoptosis level was decreased (P < 0.05). (3) In addition, the in vitro subcutaneous tumor formation experiment of nude mice showed that compared with the empty control group, the mass and growth rate of subcutaneous tumors formed by U87MG cells in the choline kinase alpha silencing lentivirus group were significantly reduced (P < 0.000 1). After Mdivi-1 treatment, the mass and growth rate of tumors were significantly increased (P < 0.000 1). (4) The results show that choline kinase alpha silencing affects the proliferation and apoptosis of glioma cells by inducing mitochondrial dysfunction.
holine kinase alpha  /  glioblastoma  /  mitochondrial function  /  Mdivi-1  /  reactive oxygen species  /  mitochondrial membrane potential  /  proliferation  /  apoptosis
赵阳, 李嘉麟, 吴箫, 邹有瑞, 刘阳, 马辉. 胆碱激酶α沉默诱导线粒体功能障碍影响胶质瘤细胞的增殖和凋亡. 中国组织工程研究, 2026 , 30 (1) : 130 -138 . DOI: 10.12307/2026.540
. Choline kinase alpha silencing affects proliferation and apoptosis in glioma cells by inducing mitochondrial dysfunction[J]. Chinese Journal of Tissue Engineering Research, 2026 , 30 (1) : 130 -138 . DOI: 10.12307/2026.540
  • 国家自然科学基金项目
  • 宁夏自然科学基金项目
  • 宁夏自然科学基金项目
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doi: 10.12307/2026.540
  • 首发时间:2025-05-30
  • 出版时间:2026-01-08
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  • 录用日期:2025-04-03
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国家自然科学基金项目
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作者信息
    1.夏医科大学,宁夏回族自治区银川市 750004
    2.津市天津医院,天津市 300000
    3.夏医科大学总医院,宁夏回族自治区银川市 750004
    4.夏医科大学总医院,宁夏回族自治区银川市 750004

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红菇科 Russulaceae 3 23 11.00 小皮伞属 Marasmius 6 2.87
小菇属 Mycena 11 5.26
光柄菇属 Pluteus 5 2.39
红菇属 Russula 17 8.13
栓菌属 Trametes 5 2.39
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