[1]林兴伟,戚新春.干扰TRIAP1表达增强口腔鳞状细胞癌细胞对顺铂敏感性实验研究[J].陕西医学杂志,2022,51(2):131-135,150.[doi:DOI:10.3969/j.issn.1000-7377.2022.02.001]
　LIN Xingwei,QI Xinchun.Interference with the expression of TRIAP1 enhances the sensitivity of oral squamous cell carcinoma cells to cisplatin[J].,2022,51(2):131-135,150.[doi:DOI:10.3969/j.issn.1000-7377.2022.02.001]
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干扰TRIAP1表达增强口腔鳞状细胞癌细胞对顺铂敏感性实验研究
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《陕西医学杂志》[ISSN:1000-7377/CN:61-1281/TN]

卷:
51
期数:
2022年2期
页码:
131-135,150
栏目:
基础研究
出版日期:
2022-02-05

文章信息/Info

Title:
Interference with the expression of TRIAP1 enhances the sensitivity of oral squamous cell carcinoma cells to cisplatin
作者:
林兴伟1; 戚新春2
(1.空军军医大学第三附属医院急诊与综合临床科,陕西 西安 710032; 2.陕西省肿瘤医院头颈肿瘤科,陕西 西安 710061)
Author(s):
LIN Xingwei; QI Xinchun
(Department of Emergency and Comprehensive Clinical Medicine,the Third Affiliated Hospital of Air Force Medical University,Xi'an 710032,China)
关键词:
口腔鳞状细胞癌;  肿瘤蛋白53调控的细胞凋亡抑制剂1;  顺铂;  细胞凋亡;  敏感性;  蛋白表达
Keywords:
Oral squamous cell carcinoma;  Tumor protein 53-regulated inhibitor of apoptosis 1;  Cisplatin;  Apoptosis;  Sensitivity;  Protein expression
分类号:
R 739.8
DOI:
DOI:10.3969/j.issn.1000-7377.2022.02.001
文献标志码:
A
摘要:
目的:探讨肿瘤蛋白53调控的细胞凋亡抑制剂1(TRIAP1)对口腔鳞状细胞癌(OSCC)细胞顺铂(DDP)敏感性的影响及作用机制。方法:常规培养OSCC细胞系Cal-27细胞,采用分次DDP诱导递增法建立DDP耐药OSCC细胞株(DDP-Cal-27),MTS检测DDP-Cal-27细胞对DDP的敏感性,Western blot检测DDP-Cal-27细胞中TRIAP1的表达。并采用TRIAP1干扰慢病毒构建TRIAP1敲低的DDP耐药OSCC细胞株(sh-TRIAP1)及对照无关序列感染的DDP耐药OSCC细胞株(sh-NC),Western blot检测sh-TRIAP1细胞中TRIAP1的表达,MTS检测sh-TRIAP1细胞对DDP的敏感性。sh-NC组和sh-TRIAP1组细胞经DDP处理后,平板克隆检测各组细胞平板克隆形成能力,流式细胞仪检测各组细胞凋亡率,Western blot检测各组细胞中凋亡蛋白Caspase 9和Caspase 3蛋白的表达,耐药相关蛋白P-gp和ABCG2的表达。结果:与Cal-27细胞相比,DDP-Cal-27细胞对DDP的敏感性降低,DDP-Cal-27细胞中TRIAP1的表达增加(均P<0.05)。TRIAP1干扰慢病毒感染DDP-Cal-27细胞后,与sh-NC组相比,sh-TRIAP1组细胞中TRIAP1的表达降低和对DDP的敏感性增强(均P<0.05)。与sh-NC组相比,DDP处理的sh-TRIAP1组细胞平板克隆形成能力降低,细胞凋亡率增加(均P<0.05),sh-TRIAP1组细胞中凋亡蛋白Caspase 9和Caspase 3蛋白的表达增加,耐药相关蛋白P-gp和ABCG2表达降低(P<0.05)。结论:TRIAP1可能通过调控凋亡相关蛋白增加OSCC细胞DDP敏感性,是治疗OSCC的潜在靶点。
Abstract:
Objective:To investigate the effect of tumor protein 53-regulated inhibitor of apoptosis 1(TRIAP1)on the sensitivity of oral squamous cell carcinoma(OSCC)cells to cisplatin(DDP)and its mechanism of action.Methods:The OSCC cell line Cal-27 was routinely cultured,and the DDP-resistant OSCC cell line(DDP-Cal-27)was established by the fractional DDP induction method.MTS was used to detect the sensitivity of DDP-Cal-27 cells to DDP,and Western blot was used to detect the expression of TRIAP1 in DDP-Cal-27 cells.TRIAP1 interfering lentivirus was used to construct TRIAP1 knockdown DDP-resistant OSCC cell line(sh-TRIAP1)and control unrelated sequence infected DDP-resistant OSCC cell line(sh-NC).The expression of TRIAP1 in sh-TRIAP1 cells was detected by Western blot and the sensitivity of sh-TRIAP1 cells to DDP was detected by MTS.After the cells in the sh-NC group and sh-TRIAP1 group were treated with DDP,the plate clone was used to detect the plate clone formation ability of each group cells,the flow cytometer was used to detect the apoptosis rate of each group cells,and the Western blot was used to detect the apoptotic protein(Caspase 9 and Caspase 3 proteins)expression and resistance-related protein(P-gp and ABCG2)expressioin in each group of cells.Results:Compared with Cal-27 cells,the sensitivity of DDP-Cal-27 cells to DDP was decreased,and the expression of TRIAP1 in DDP-Cal-27 cells was increased(all P<0.05).After TRIAP1 interfered with lentivirus infection of DDP-Cal-27 cells,compared with the sh-NC group,the expression of TRIAP1 in the sh-TRIAP1 group was reduced and the sensitivity to DDP was enhanced(all P<0.05).Compared with the sh-NC group,the cell plate clone formation ability of DDP-treated sh-TRIAP1 group was decreased,and the apoptosis rate was increased,and the expression of Caspase 9 and Caspase 3 in the sh-TRIAP1 group were increased,and the expression of P-gp and ABCG2 were decreased(all P<0.05). Conclusion:TRIAP1 may increase the DDP sensitivity of OSCC cells by regulating apoptosis-related proteins,and is a potential target for the treatment of OSCC.

参考文献/References:

[1] 白 雪,张 斌,汪 潇,等.miR-637调控RING1表达抑制口腔鳞癌Tac-8113细胞增殖实验研究[J].陕西医学杂志,2020,49(8):923-927.
[2] Siegel RL,Miller KD,Jemal A.Cancer statistics,2018[J].CA Cancer J Clin,2018,68(1):7-30.
[3] Wang Y,Xie D,Pan J,et al.A near infrared light-triggered human serum albumin drug delivery system with coordination bonding of indocyanine green and cisplatin for targeting photochemistry therapy against oral squamous cell cancer[J].Biomater Sci,2019,7(12):5270-5282.
[4] 孙晓冉,孙剑经,张林西.肿瘤多药耐药机制的研究进展[J].现代肿瘤医学,2017,25(1):164-166.
[5] Li Y,Tang X,He Q,et al.Overexpression of mitochondria mediator gene TRIAP1 by miR-320b loss is associated with progression in nasopharyngeal carcinoma[J].PLoS Genet,2016,12(7):1006183.
[6] Zhang J,Cong R,Zhao K,et al.High TRIAP1 expression in penile carcinoma is associated with high risk of recurrence and poor survival[J].Ann Transl Med,2019,7(14):330.
[7] Cai P,Li J,Chen G,et al.MicroRNA-107 may regulate lung cancer cell proliferation and apoptosis by targeting TP53 regulated inhibitor of apoptosis 1[J].Oncol Lett,2020,19(3):1958-1966.
[8] Fook-Alves VL,Oliveira MB,Zanatta DB,et al.TP53 regulated inhibitor of apoptosis 1(TRIAP1)stable silencing increases late apoptosis by upregulation of Caspase 9 and APAF1 in RPMI8226 multiple myeloma cell line[J].Biochim Biophys Acta,2016,1862(6):1105-1110.
[9] Zhang TM.TRIAP1 inhibition activates the cytochrome C/Apaf-1/Caspase-9 signaling pathway to enhance human ovarian cancer sensitivity to cisplatin[J].Chemotherapy,2019,64(3):119-128.
[10] Ketteler J,Panic A,Reis H,et al.Progression-related loss of stromal caveolin 1 levels mediates radiation resistance in prostate carcinoma via the apoptosis inhibitor TRIAP1[J].J Clin Med,2019,8(3):348.
[11] Na C,Li X,Zhang J,et al.miR-107 targets TRIAP1 to regulate oral squamous cell carcinoma proliferation and migration[J].Int J Clin Exp Pathol,2019,12(5):1820-1825.
[12] 周建军,王国栋.口腔鳞状细胞癌铂类药物耐药分子机制研究进展[J].中国肿瘤生物治疗杂志,2019,26(11):1288-1292.
[13] Adams C,Cazzanelli G,Rasul S,et al.Apoptosis inhibitor TRIAP1 is a novel effector of drug resistance[J].Oncol Rep,2015,34(1):415-422.
[14] Hao CC,Luo JN,Xu CY,et al.TRIAP1 knockdown sensitizes non-small cell lung cancer to ionizing radiation by disrupting redox homeostasis[J].Thorac Cancer,2020,11(4):1015-1025.
[15] 梁 凯,曹秉振.线粒体调控的细胞凋亡研究进展[J].生物医学工程与临床,2014,18(5):501-505.
[16] Fang Y,Li J,Wu Y,et al.Costunolide inhibits the growth of OAW42-A multidrug-resistant human ovarian cancer cells by activating apoptotic and autophagic pathways,production of reactive oxygen species(ROS),cleaved caspase-3 and cleaved caspase-9[J].Med Sci Monit,2019,25(5):3231-3237.
[17] Lu X,Wang Z,Huang H,et al.Hedgehog signaling promotes multidrug resistance by regulation of ABC transporters in oral squamous cell carcinoma[J].J Oral Pathol Med,2020,49(9):897-906.
[18] Sharma ND,Nickl CK,Kang H,et al.Epigenetic silencing of SOCS5 potentiates JAK-STAT signaling and progression of T-cell acute lymphoblastic leukemia[J].Cancer Sci,2019,110(6):1931-1946.
[19] 李希博,刘丽伟,李 娜,等.口腔鳞状细胞癌的血清生物标志物鉴定及代谢紊乱特征研究[J].中华口腔医学杂志,2021,56(9):926-932.
[20] 胡勤刚,赵星星.口腔鳞状细胞癌肿瘤相关成纤维细胞的研究进展[J].口腔医学研究,2020,36(4):309-313.

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备注/Memo

备注/Memo:
基金项目:陕西省重点研发计划项目(2019SF-140)
更新日期/Last Update: 2022-02-09