[1]何海新,卢永伟,林翠波,等.PTEN抑制剂逆转靶向microRNA-24抑制宫颈癌发生、发展的机制探索[J].福建医药杂志,2024,46(07):69-71.[doi:10.20148/j.fmj.2024.07.022]
　HE Haixin,LU Yongwei,LIN Cuibo,et al.Mechanism exploration of reverse targeting of microRNA-24 by PTEN inhibitors to inhibit the occurrence and development of cervical cancer[J].FUJIAN MEDICAL JOURNAL,2024,46(07):69-71.[doi:10.20148/j.fmj.2024.07.022]
点击复制

PTEN抑制剂逆转靶向microRNA-24抑制宫颈癌发生、发展的机制探索()
分享到：

《福建医药杂志》[ISSN:1002-2600/CN:35-1071/R]

卷:
46
期数:
2024年07期
页码:
69-71
栏目:
基础研究
出版日期:
2024-11-20

文章信息/Info

Title:
Mechanism exploration of reverse targeting of microRNA-24 by PTEN inhibitors to inhibit the occurrence and development of cervical cancer
文章编号:
1002-2600(2024)07-0069-03
作者:
何海新; 卢永伟; 林翠波; 吴宏清
福建医科大学肿瘤临床医学院 福建省肿瘤医院妇科,福州 350014
Author(s):
HE Haixin; LU Yongwei; LIN Cuibo; WU Hongqing
Department of Gynecology, Fujian Cancer Hospital, Clinical Oncology School of Fujian Medical University, Fuzhou, Fujian 350014, China
关键词:
miR-24;  宫颈癌;  调控;  张力蛋白同源磷酸酶基因
Keywords:
miR-24;  cervical cancer;  regulation;  PTEN
分类号:
R734.33
DOI:
10.20148/j.fmj.2024.07.022
文献标志码:
A
摘要:
目的 探讨microRNA-24(miR-24)在宫颈癌(CC)的发生、形成中的作用和调控机制。方法 使用HELA S3细胞系进行裸鼠皮下成瘤实验,采用免疫组织化学(IHC)检测细胞周期蛋白D1(Cyclin D1)、增殖细胞相关蛋白Ki-67、上皮钙黏蛋白(E-cadherin)和波形蛋白(Vimentin)的表达来研究miR-24和张力蛋白同源磷酸酶基因(PTEN)对肿瘤生长的影响。结果 miR-24抑制剂组肿瘤重量降低; Cyclin D1、Ki-67表达量降低,细胞增殖能力被抑制; E-cadherin表达增强,Vimentin表达被抑制。miR-24抑制剂+ si-PTEN组的检测结果显示:si-PTEN逆转了miR-24抑制剂的效果。结论 miR-24抑制剂抑制CC细胞系增殖和侵袭能力,而PTEN的下调可逆转miR-24抑制剂对CC细胞系增殖和侵袭的影响。靶向miR-24可能为预防和治疗CC提供一种新的治疗策略。
Abstract:
Objective To investigate the role of microRNA-24(miR-24)in the pathogenesis, formation and regulation of cervical cancer(CC).Methods Subcutaneous tumor formation test of nude mice was conducted with HELA S3 cell line.The expressions of Cyclin D1, Ki-67, E-cadherin and Vimentin were detected by immunohistochemistry(IHC)to study the effects of miR-24 and PTEN on tumor growth.Results The tumor weight was significantly inhibited in miR-24 inhibitor group.The expression levels of Cyclin D1 and Ki-67 decreased, and cell proliferation was inhibited.E-cadherin expression was enhanced, while Vimentin expression was inhibited.The detection results of miR-24 inhibitor + si-PTEN group showed that si-PTEN reversed the effect of miR-24 inhibitor.Conclusion miR-24 inhibitors significantly inhibit the proliferation and invasion of CC cell lines, and down-regulation of PTEN can reverse the effects of miR-24 inhibitors on the proliferation and invasion of CC cell lines.Targeting miR-24 may provide a new therapeutic strategy for the prevention and treatment of CC.

参考文献/References:

[1] HU M, ZHU S, XIONG S, et al.MicroRNAs and the PTEN/PI3K/Akt pathway in gastric cancer[J].Oncology Reports,2019, 41(3): 1439-1454.
[2] LI Y Q, LU J H, BAO X M, et al.MiR-24 functions as a tumor suppressor in nasopharyngeal carcinoma through targeting FSCN1[J].Journal of Experimental & Clinical Cancer Research, 2015, 34: 1-9.
[3] LIU R, ZHANG H, WANG X, et al.The mir-24-Bim path-way promotes tumor growth and angiogenesis in pancreatic carcinoma[J].Oncotarget, 2015, 6(41):43831-43842.
[4] VOLINIA S, CALIN G A, LIU C G, et al.A microRNA expressionsignature of human solid tumors defines cancer gene targets[J].Proc Natl Acad Sci USA,2006,103(7): 2257-2261.
[5] TUT V M, BRAITHWAITE K L, ANGUS B, et al.Cyclin D1 expression in transitional cell carcinoma of the bladder: correlation with p53,wsf1,pRb and Ki67[J].Br J Cancer, 2001, 84(2):270.
[6] SHOU Y, WANG X, CHEN C, et al.Exosomal miR-301a-3p from esophageal squamous cell carcinoma cells promotes angiogenesis by inducing M2 polarization of macrophages via the PTEN/PI3K/AKT signaling pathway[J].Cancer Cell Int, 2022, 22(1):153.
[7] HE T, SUN Y, ZHANG Y, et al.MicroRNA-200b and microRNA-200c are up-regulated in PCOS granulosa cell and inhibit KGN cell proliferation via targeting PTEN[J].Reprod Biol Endocrinol, 2019, 17(1):68.
[8] 杨剑,糜漫天.细胞周期素D1与肿瘤研究进展[J].国外医学(肿瘤学分册),2003,30(5):336-339.
[9] KANYLMAZ G, YAVUZ B B, AKTAN M, et al.Prognostic importance of Ki-67 in breast cancer and its relationship with other prognostic factors[J].European Journal of Breast Health, 2019, 15(4): 256.
[10] WONG A S T, GUMBINER B M.Adhesion-independent mechanism for suppression of tumor cell invasion by E-cadherin[J].The Journal of Cell Biology, 2003, 161(6): 1191-1203.
[11] IVASKA J.Vimentin: Central hub in EMT induction[J].Small GTPases, 2011, 2(1): 1436-1448.
[12] HE H, LIN C, LU Y, et al.Knockdown of miR-24 Suppressed the tumor growth of cervical carcinoma through regulating PTEN/PI3K/AKT signaling pathway[J].Biochemical Gene-tics, 2024,62(2):1277-1290.

相似文献/References:

[1]黄 勉 林 珺 沈 张 金 琼 陶 红 吴三山 刘禹利.PAX1基因甲基化用于子宫颈癌临床应用价值探讨[J].福建医药杂志,2020,42(03):3.
　HUANG Mian,LIN Jun,SHEN Zhang,et al.Clinical application value of methylated PAX1 gene in cervical cancer[J].FUJIAN MEDICAL JOURNAL,2020,42(07):3.
[2]林智平 王 英 王兰兰 罗益平.老年宫颈癌患者外周血S100A8水平和术后认知功能障碍发生的关系[J].福建医药杂志,2020,42(05):5.
　LIN Zhiping,WANG Ying,WANG Lanlan,et al.Relationship between peripheral blood S100A8 level and postoperative cognitive dysfunction in elderly patients with cervical cancer[J].FUJIAN MEDICAL JOURNAL,2020,42(07):5.
[3]王芳,李全荣,邱琳,等.宫颈高级别上皮内瘤变及宫颈癌患者HPV检测分析[J].福建医药杂志,2021,43(01):39.

备注/Memo

备注/Memo:
基金项目:福建省卫健委科技计划项目(2020CXA014)
更新日期/Last Update: 2024-11-20