CDCA5与肿瘤

doi:10.3760/cma.j.cn371439-20200810-00007

摘要/Abstract

摘要：

姐妹染色单体凝聚发生于DNA复制时期,由黏合素调节,并且依赖于细胞分裂周期相关蛋白5(CDCA5)及黏合素的乙酰化。WAPL可以促进黏合素与DNA解离,CDCA5可以拮抗WAPL的作用,通过稳定黏合素与DNA的结合从而稳定姐妹染色单体凝聚。CDCA5 mRNA在多种肿瘤细胞株中具有较高的转录水平,提示CDCA5可能与肿瘤细胞较高的恶性增殖活性有关,并且已经在肝癌、肺癌等多种肿瘤中得到证实,CDCA5可能是肿瘤治疗的潜在靶向分子。

关键词: 肿瘤, 细胞分裂周期相关蛋白5, Sororin, 黏合素

Abstract:

Cohesion between sister chromatids occurs during DNA replication, is regulated by cohesin, and depends on acetylation of cell division cycle associated 5 (CDCA5) and cohesin. WAPL can promote dissociation of cohesin from DNA, and CDCA5 can antagonize the effect of WAPL and stabilize sister chromatids cohesion by stabilizing the binding of cohesin to DNA. CDCA5 mRNA has a high transcription level in a variety of tumor cell lines, suggesting that CDCA5 may be related to the higher malignant proliferation activity of tumor cells, and has been confirmed in various tumors such as liver cancer and lung cancer, and CDCA5 may be a potential targeted molecule for the treatment of malignant tumors.

Key words: Neoplasms, Cell division cycle associated 5, Sororin, Cohesion

何佩东, 李子坚. CDCA5与肿瘤[J]. 国际肿瘤学杂志, 2021, 48(1): 41-44.

He Peidong, Li Zijian. CDCA5 and tumors[J]. Journal of International Oncology, 2021, 48(1): 41-44.

参考文献 29

[1]	Chang IW, Lin VC, He HL, et al. CDCA5 overexpression is an indicator of poor prognosis in patients with urothelial carcinomas of the upper urinary tract and urinary bladder[J]. Am J Transl Res, 2015,7(4):710-722. pmid: 26064439
[2]	Fu G, Xu Z, Chen X, et al. CDCA5 functions as a tumor promoter in bladder cancer by dysregulating mitochondria-mediated apoptosis, cell cycle regulation and PI3k/AKT/mTOR pathway activation[J]. J Cancer, 2020,11(9):2408-2420. DOI: 10.7150/jca.35372. pmid: 32201512
[3]	Cai C, Wang W, Tu Z. Aberrantly DNA methylated-differentially expressed genes and pathways in hepatocellular carcinoma[J]. J Cancer, 2019,10(2):355-366. DOI: 10.7150/jca.27832. pmid: 30719129
[4]	Wan Z, Zhang X, Luo Y, et al. Identification of hepatocellular carcinoma-related potential genes and pathways through bioinformatic-based analyses[J]. Genet Test Mol Biomarkers, 2019,23(11):766-777. DOI: 10.1089/gtmb.2019.0063. pmid: 31633428
[5]	Chen H, Chen J, Zhao L, et al. CDCA5, transcribed by E2F1, promotes oncogenesis by enhancing cell proliferation and inhibiting apoptosis via the AKT pathway in hepatocellular carcinoma[J]. J Cancer, 2019,10(8):1846-1854. DOI: 10.7150/jca.28809. doi: 10.7150/jca.28809 pmid: 31205541
[6]	Tian Y, Wu J, Chagas C, et al. CDCA5 overexpression is an Indicator of poor prognosis in patients with hepatocellular carcinoma (HCC)[J]. BMC Cancer, 2018,18(1):1187. DOI: 10.1186/s12885-018-5072-4. doi: 10.1186/s12885-018-5072-4 pmid: 30497429
[7]	Wang J, Xia C, Pu M, et al. Silencing of CDCA5 inhibits cancer progression and serves as a prognostic biomarker for hepatocellular carcinoma[J]. Oncol Rep, 2018,40(4):1875-1884. DOI: 10.3892/or.2018.6579. doi: 10.3892/or.2018.6579 pmid: 30015982
[8]	Shen Z, Yu X, Zheng Y, et al. CDCA5 regulates proliferation in hepatocellular carcinoma and has potential as a negative prognostic marker[J]. Onco Targets Ther, 2018,11:891-901. DOI: 10.2147/OTT.S154754. pmid: 29503564
[9]	Lin Y, Liang R, Ye J, et al. A twenty gene-based gene set variation score reflects the pathological progression from cirrhosis to hepatocellular carcinoma[J]. Aging (Albany NY), 2019,11(23):11157-11169. DOI: 10.18632/aging.102518.
[10]	Zhang Z, Shen M, Zhou G. Upregulation of CDCA5 promotes gastric cancer malignant progression via influencing cyclin E1[J]. Biochem Biophys Res Commun, 2018,496(2):482-489. DOI: 10.1016/j.bbrc.2018.01.046. pmid: 29326043
[11]	Chen T, Huang Z, Tian Y, et al. Role of triosephosphate isomerase and downstream functional genes on gastric cancer[J]. Oncol Rep, 2017,38(3):1822-1832. DOI: 10.3892/or.2017.5846. doi: 10.3892/or.2017.5846 pmid: 28737830
[12]	Nguyen MH, Koinuma J, Ueda K, et al. Phosphorylation and activation of cell division cycle associated 5 by mitogen-activated protein kinase play a crucial role in human lung carcinogenesis[J]. Cancer Res, 2010,70(13):5337-5347. DOI: 10.1158/0008-5472.can-09-4372. pmid: 20551060
[13]	Wu Q, Zhang B, Sun Y, et al. Identification of novel biomarkers and candidate small molecule drugs in non-small-cell lung cancer by integrated microarray analysis[J]. Onco Targets Ther, 2019,12:3545-3563. DOI: 10.2147/ott.s198621. doi: 10.2147/OTT.S198621 pmid: 31190860
[14]	Huang J, Li Y, Lu Z, et al. Analysis of functional hub genes identifies CDC45 as an oncogene in non-small cell lung cancer-a short report[J]. Cell Oncol (Dordr), 2019,42(4):571-578. DOI: 10.1007/s13402-019-00438-y.
[15]	Ladurner R, Kreidl E, Ivanov MP, et al. Sororin actively maintains sister chromatid cohesion[J]. EMBO J, 2016,35(6):635-653. DOI: 10.15252/embj.201592532. pmid: 26903600
[16]	Zhang N, Pati D. C-terminus of Sororin interacts with SA2 and regulates sister chromatid cohesion[J]. Cell Cycle, 2015,14(6):820-826. DOI: 10.1080/15384101.2014.1000206. pmid: 25608232
[17]	Nishiyama T, Ladurner R, Schmitz J, et al. Sororin mediates sister chromatid cohesion by antagonizing Wapl[J]. Cell, 2010,143(5):737-749. DOI: 10.1016/j.cell.2010.10.031. doi: 10.1016/j.cell.2010.10.031 pmid: 21111234
[18]	Nishiyama T, Sykora MM, Huis in't Veld PJ, et al. Aurora B and Cdk1 mediate Wapl activation and release of acetylated cohesin from chromosomes by phosphorylating Sororin[J]. Proc Natl Acad Sci U S A, 2013,110(33):13404-13409. DOI: 10.1073/pnas.1305020110. doi: 10.1073/pnas.1305020110 pmid: 23901111
[19]	Borton MT, Rashid MS, Dreier MR, et al. Multiple levels of regulation of sororin by Cdk1 and Aurora B[J]. J Cell Biochem, 2016,117(2):351-360. DOI: 10.1002/jcb.25277. doi: 10.1002/jcb.25277 pmid: 26177583
[20]	Zhang N, Pati D. Sororin is a master regulator of sister chromatid cohesion and separation[J]. Cell Cycle, 2012,11(11):2073-2083. DOI: 10.4161/cc.20241. doi: 10.4161/cc.20241 pmid: 22580470
[21]	Liu J, Meng H, Li S, et al. Identification of potential biomarkers in association with progression and prognosis in epithelial ovarian cancer by integrated bioinformatics analysis[J]. Front Genet, 2019,10:1031. DOI: 10.3389/fgene.2019.01031. pmid: 31708970
[22]	Shen A, Liu L, Chen H, et al. Cell division cycle associated 5 promotes colorectal cancer progression by activating the ERK signaling pathway[J]. Oncogenesis, 2019,8(3):19. DOI: 10.1038/s41389-019-0123-5. pmid: 30808873
[23]	Xu J, Zhu C, Yu Y, et al. Systematic cancer-testis gene expression analysis identified CDCA5 as a potential therapeutic target in esophageal squamous cell carcinoma[J]. EBioMedicine, 2019,46:54-65. DOI: 10.1016/j.ebiom.2019.07.030. doi: 10.1016/j.ebiom.2019.07.030 pmid: 31324603
[24]	Zhou Q, Ren J, Hou J, et al. Co-expression network analysis identified candidate biomarkers in association with progression and prognosis of breast cancer[J]. J Cancer Res Clin Oncol, 2019,145(9):2383-2396. DOI: 10.1007/s00432-019-02974-4. doi: 10.1007/s00432-019-02974-4 pmid: 31280346
[25]	Fu Y, Zhou QZ, Zhang XL, et al. Identification of hub genes using co-expression network analysis in breast cancer as a tool to predict different stages[J]. Med Sci Monit, 2019,25:8873-8890. DOI: 10.12659/msm.919046. doi: 10.12659/MSM.919046 pmid: 31758680
[26]	Phan NN, Wang CY, Li KL, et al. Distinct expression of CDCA3, CDCA5, and CDCA8 leads to shorter relapse free survival in breast cancer patient[J]. Oncotarget, 2018,9(6):6977-6992. DOI: 10.18632/oncotarget.24059. pmid: 29467944
[27]	Kato T, Lee D, Wu L, et al. SORORIN and PLK1 as potential the-rapeutic targets in malignant pleural mesothelioma[J]. Int J Oncol, 2016,49(6):2411-2420. DOI: 10.3892/ijo.2016.3765. pmid: 27840913
[28]	Tokuzen N, Nakashiro K, Tanaka H, et al. Therapeutic potential of targeting cell division cycle associated 5 for oral squamous cell carcinoma[J]. Oncotarget, 2016,7(3):2343-2353. DOI: 10.18632/oncotarget.6148. doi: 10.18632/oncotarget.6148 pmid: 26497678
[29]	Xu T, Ma M, Dai J, et al. Gene expression screening identifies CDCA5 as a potential therapeutic target in acral melanoma[J]. Hum Pathol, 2018,75:137-145. DOI: 10.1016/j.humpath.2018.02.009. pmid: 29452217

CDCA5与肿瘤

CDCA5 and tumors

RichHTML

PDF

可视化

摘要/Abstract

引用本文

使用本文

参考文献 29

相关文章 15

编辑推荐

Metrics

本文评价

[1]	刘娜, 寇介丽, 杨枫, 刘桃桃, 李丹萍, 韩君蕊, 杨立洲. 血清miR-106b-5p、miR-760联合低剂量螺旋CT诊断早期肺癌的临床价值[J]. 国际肿瘤学杂志, 2024, 51(6): 321-325.
[2]	杨蜜, 别俊, 张加勇, 邓佳秀, 唐组阁, 卢俊. 局部晚期可切除食管癌新辅助治疗疗效及预后分析[J]. 国际肿瘤学杂志, 2024, 51(6): 332-337.
[3]	袁健, 黄燕华. Hp-IgG抗体联合血清DKK1、sB7-H3对早期胃癌的诊断价值[J]. 国际肿瘤学杂志, 2024, 51(6): 338-343.
[4]	陈红健, 张素青. 血清miR-24-3p、H2AFX与肝癌患者临床病理特征及术后复发的关系研究[J]. 国际肿瘤学杂志, 2024, 51(6): 344-349.
[5]	郭泽浩, 张俊旺. PFDN及其亚基在肿瘤发生发展中的作用[J]. 国际肿瘤学杂志, 2024, 51(6): 350-353.
[6]	张百红, 岳红云. 新作用机制的抗肿瘤药物进展[J]. 国际肿瘤学杂志, 2024, 51(6): 354-358.
[7]	许凤琳, 吴刚. EBV在鼻咽癌肿瘤免疫微环境和免疫治疗中的研究进展[J]. 国际肿瘤学杂志, 2024, 51(6): 359-363.
[8]	王盈, 刘楠, 郭兵. 抗体药物偶联物在转移性乳腺癌治疗中的研究进展[J]. 国际肿瘤学杂志, 2024, 51(6): 364-369.
[9]	张蕊, 褚衍六. 基于FIT与肠道菌群的结直肠癌风险评估模型的研究进展[J]. 国际肿瘤学杂志, 2024, 51(6): 370-375.
[10]	高凡, 王萍, 杜超, 褚衍六. 肠道菌群与结直肠癌非手术治疗的相关研究进展[J]. 国际肿瘤学杂志, 2024, 51(6): 376-381.
[11]	王丽, 刘志华, 杨伟洪, 蒋凤莲, 李全泳, 宋浩杰, 鞠文东. ROS1突变肺腺鳞癌合并脑梗死为主要表现的Trousseau综合征1例[J]. 国际肿瘤学杂志, 2024, 51(6): 382-384.
[12]	刘静, 刘芹, 黄梅. 基于SMOTE算法的食管癌放化疗患者肺部感染的预后模型构建[J]. 国际肿瘤学杂志, 2024, 51(5): 267-273.
[13]	杨琳, 路宁, 温华, 张明鑫, 朱琳. 炎症负荷指数与胃癌临床关系研究[J]. 国际肿瘤学杂志, 2024, 51(5): 274-279.
[14]	王俊毅, 洪楷彬, 纪荣佳, 陈大朝. 癌结节对结直肠癌根治性切除术后肝转移的影响[J]. 国际肿瘤学杂志, 2024, 51(5): 280-285.
[15]	张宁宁, 杨哲, 檀丽梅, 李振宁, 王迪, 魏永志. 宫颈细胞DNA倍体分析联合B7-H4和PKCδ对宫颈癌的诊断价值[J]. 国际肿瘤学杂志, 2024, 51(5): 286-291.