[1]高晨峰,刘 斌,陈小凤,等.JS-K对口腔鳞状细胞癌H157和CAL-27细胞增殖与凋亡的影响及机制实验研究[J].陕西医学杂志,2023,52(12):1631-1641,1647.[doi:DOI:10.3969/j.issn.1000-7377.2023.12.003]
　GAO Chenfeng,LIU Bin,CHEN Xiaofeng,et al.Effects and mechanism of JS-K on proliferation and apoptosis of oral squamous cell carcinoma H157 and CAL-27 cells[J].,2023,52(12):1631-1641,1647.[doi:DOI:10.3969/j.issn.1000-7377.2023.12.003]
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JS-K对口腔鳞状细胞癌H157和CAL-27细胞增殖与凋亡的影响及机制实验研究
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《陕西医学杂志》[ISSN:1000-7377/CN:61-1281/TN]

卷:
52
期数:
2023年12期
页码:
1631-1641,1647
栏目:
基础研究
出版日期:
2023-12-05

文章信息/Info

Title:
Effects and mechanism of JS-K on proliferation and apoptosis of oral squamous cell carcinoma H157 and CAL-27 cells
作者:
高晨峰1; 刘 斌1; 陈小凤1; 廖卫国1; 黄小杰1; 杨 腾2; 于立明3; 兰 青3
(1.广东医科大学附属医院肝胆外科,广东 湛江 524001; 2.广东医科大学附属医院临床医学研究中心,广东 湛江 524001; 3.广东医科大学附属医院口腔科,广东 湛江 524001)
Author(s):
GAO Chenfeng; LIU Bin; CHEN Xiaofeng; LIAO Weiguo; HUANG Xiaojie; YANG Teng; YU Liming; LAN Qing
(Department of Hepatobiliary Surgery,Affiliated Hospital of Guangdong Medical University,Zhanjiang 524001,China)
关键词:
口腔鳞状细胞癌;  JS-K;  细胞周期;  细胞凋亡;  丝裂原活化蛋白激酶;  活性氧
Keywords:
Oral squamous cell carcinoma;  JS-K;  Cell cycle;  Apoptosis;  Mitogen-activated protein kinase;  Reactive oxygen species
分类号:
R 739.85
DOI:
DOI:10.3969/j.issn.1000-7377.2023.12.003
文献标志码:
A
摘要:
目的:探讨一氧化氮(NO)前体化合物(JS-K)对口腔鳞状细胞癌(OSCC)H157和CAL-27细胞增殖与凋亡的影响,并分析相关机制。方法:采用细胞活力与平板克隆实验检测JS-K对OSCC细胞增殖能力的影响。采用流式细胞术检测细胞周期与细胞凋亡,以及半胱氨酸蛋白酶3/7(Caspase-3/7)活性测定评估JS-K对OSCC细胞周期与凋亡的影响。检测JS-K干预后OSCC细胞中ROS生成情况。采用亚细胞分离技术与Western blot探索JS-K诱导OSCC细胞周期停滞与细胞凋亡的机制。结果:JS-K通过p38丝裂原活化蛋白激酶(MAPK)信号通路抑制OSCC细胞的增殖,诱导细胞凋亡和细胞周期阻滞。此外,JS-K激活的p38 MAPK信号通路导致OSCC细胞中ROS增加,并诱导细胞周期阻滞在G2/M期。结论:JS-K通过p38 MAPK信号通路调控ROS,诱导OSCC细胞周期阻滞在G2/M期并凋亡,最终抑制OSCC细胞增殖。JS-K可能为一种治疗OSCC的潜在药物。
Abstract:
Objective:To investigate the effects of nitric oxide(NO)precursor compounds(JS-K)on the proliferation and apoptosis of oral squamous cell carcinoma(OSCC)H157 and CAL-27 cells,and to explore the related mechanisms.Methods:The effect of JS-K on OSCC cell proliferation was determined by cell viability and colony formation assay.The cell cycle and apoptosis were detected by flow cytometry,and the effect of JS-K on OSCC cell cycle and apoptosis was evaluated by Caspase-3/7 activity.ROS detection was used to detect ROS production in OSCC cells after JS-K application.Subcell separation techniques and Western blot were used to explore the mechanism of JS-K induced OSCC cell cycle arrest and cell apoptosis.Results:JS-K inhibited OSCC cell proliferation,induced cell apoptosis and cell cycle arrest through p38 MAPK signaling pathway.In addition,the JS-K-activated p38 MAPK signaling pathway leads to an increase in ROS in OSCC cells and induces cell cycle arrest in the G2/M phase.Conclusion:JS-K regulates ROS through p38 MAPK signaling pathway,inducing cell cycle arrest in G2/M phase and apoptosis,and finally inhibiting OSCC cell proliferation.JS-K may be a potential treatment for OSCC.

参考文献/References:

[1] 高 宾,王春花,李雅琪,等.长链非编码RNA在口腔鳞状细胞癌及其微环境中的作用研究进展[J].陕西医学杂志,2022,51(11):1458-1461.
[2] 施 健,胡千慧,张雪杰.口腔鳞癌组织长链非编码RNA LINC01605表达与临床病理特征关系研究[J].陕西医学杂志,2022,51(5):617-620.
[3] Zhang L,Meng X,Zhu XW,et al.Long non-coding RNAs in Oral squamous cell carcinoma:Biologic function,mechanisms and clinical implications[J].Mol Cancer,2019,18(1):102.
[4] Wang H,Luo Q,Feng X,et al.NLRP3 promotes tumor growth and metastasis in human oral squamous cell carcinoma[J].BMC Cancer,2018,18(1):500.
[5] Song L,Han X,Jia C,et al.Porcine reproductive and respiratory syndrome virus inhibits MARC-145 proliferation via inducing apoptosis and G2/M arrest by activation of Chk/Cdc25C and p53/p21 pathway[J].Virol J,2018,15(1):169.
[6] Chu Q,Gu X,Zheng Q,et al.Mitochondrial mechanisms of apoptosis and necroptosis in liver diseases[J].Anal Cell Pathol(Amst),2021,2021:8900122.
[7] 李 琨,张华湘,董素阁,等.胡桃醌对口腔鳞癌Tac8113细胞增殖与凋亡的作用及机制探究[J].中华中医药学刊,2022,40(4):107-111,262.
[8] Suski JM,Braun M,Strmiska V,et al.Targeting cell-cycle machinery in cancer[J].Cancer Cell,2021,39(6):759-778.
[9] Guo YJ,Pan WW,Liu SB,et al.ERK/MAPK signalling pathway and tumorigenesis[J].Exp Ther Med,2020,19(3):1997-2007.
[10] 汪 楠,李 岩.和胃反流康对胆汁反流性胃炎大鼠胃黏膜p38 MAPK蛋白及COX-2 mRNA表达的影响[J].长春中医药大学学报,2021,37(6):1269-1272.
[11] Wang Y,Qi H,Liu Y,et al.The double-edged roles of ROS in cancer prevention and therapy[J].Theranostics,2021,11(10):4839-4857.
[12] Mirzaei S,Hushmandi K,Zabolian A,et al.Elucidating role of reactive oxygen species(ROS)in cisplatin chemotherapy:A focus on molecular pathways and possible therapeutic strategies[J].Molecules,2021,26(8):2382.
[13] Teppo HR,Soini Y,Karihtala P.Reactive oxygen species-mediated mechanisms of action of targeted cancer therapy[J].Oxid Med Cell Longev,2017,2017:1485283.
[14] Tan G,Wu A,Li Z,et al.A review of the relatively complex mechanism of JS-K induced apoptosis in cancer cells[J].Transl Cancer Res,2019,8(4):1602-1608.
[15] Liu L,Huang Z,Chen J,et al.Protein phosphatase 2A mediates JS-K-induced apoptosis by affecting Bcl-2 family proteins in human hepatocellular carcinoma HepG2 cells[J].J Cell Biochem,2018,119(8):6633-6643.
[16] Qiu M,Zhang S,Ke L,et al.JS-K enhances chemosensitivity of prostate cancer cells to Taxol via reactive oxygen species activation[J].Oncol Lett,2019,17(1):757-764.
[17] Song Z,Yin Y,Hao S,et al.JS-K induces G2/M phase cell cycle arrest and apoptosis in A549 and H460 cells via the p53/p21WAF1/CIP1 and p27KIP1 pathways[J].Oncol Rep,2019,41(6):3475-3487.
[18] 杨雪丽,薛建华,陈天阳,等.苍术酮对肝癌HepG2细胞活性、凋亡的影响及其相关机制[J].临床肝胆病杂志,2021,37(11):2589-2594.
[19] Sekar G,Ojoawo A,Moldoveanu T.Protein-protein and protein-lipid interactions of pore-forming Bcl-2 family proteins in apoptosis initiation[J].Biochem Soc Trans,2022,50(3):1091-1103.
[20] Wang J,Huangfu M,Li X,et al.Osthole induces apoptosis and Caspase-3/GSDME-dependent pyroptosis via NQO1-mediated ROS generation in hela cells[J].Oxid Med Cell Longev,2022,2022:8585598.
[21] Liu K,Zheng M,Lu R,et al.The role of CDC25C in cell cycle regulation and clinical cancer therapy:A systematic review[J].Cancer Cell Int,2020,20:213.
[22] Zhang G,He J,Ye X,et al.Beta-thujaplicin induces autophagic cell death,apoptosis,and cell cycle arrest through ROS-mediated Akt and p38/ERK MAPK signaling in human hepatocellular carcinoma[J].Cell Death Dis,2019,10(4):255.
[23] Whitaker RH,Cook JG.Stress relief techniques:P38 MAPK determines the balance of cell cycle and apoptosis pathways[J].Biomolecules,2021,11(10):1444.
[24] Kudaravalli S,Den-Hollander P,Mani SA.Role of p38 MAP kinase in cancer stem cells and metastasis[J].Oncogene,2022,41(23):3177-3185.
[25] Zhang M,Qu J,Gao Z,et al.Timosaponin AⅢ induces G2/M arrest and apoptosis in breast cancer by activating the ATM/Chk2 and p38 MAPK signaling pathways[J].Front Pharmacol,2020,11:601468.
[26] Korbecki J,Siminska D,Gassowska-Dobrowolska M,et al.Chronic and cycling hypoxia:Drivers of cancer chronic inflammation through HIF-1 and NF-kappaB activation:A review of the molecular mechanisms[J].Int J Mol Sci,2021,22(19):10701.

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备注/Memo

备注/Memo:
基金项目:广东省基础与应用基础研究基金资助项目(2019A1515110952); 广东医科大学科研基金资助项目(M2017001); 广东医科大学附属医院博士基金资助项目(2017031798)
更新日期/Last Update: 2023-12-05