Y盒结合蛋白1与上皮-间质转化

摘要/Abstract

摘要：在上皮间质转化（EMT)过程中，细胞间连接被破坏，细胞失去顶底极性，获得抗凋亡能力及迁移、侵袭能力。Y盒结合蛋白1（YB1）是冷休克蛋白超家族的一员，包含结构和功能高度保守的冷休克结构域。研究表明，YB1可以通过调控EMT促进肿瘤的发生发展。在YB1介导的EMT中，多种转录因子及信号通路发挥着重要作用。

关键词:Y盒结合蛋白质1,细胞转化,肿瘤,转录因子,信号传导

Abstract:In the process of epithelialmesenchymal transition (EMT), cellcell adherence is disrupted, apicobasal polarity is lost, the ability of antiapoptosis, migration and invasion is acquired. Yboxbinding protein 1 (YB1) is a member of the coldshock protein superfamily, containing a structurally and functionally conserved cold shock domain. Studies indicate that YB1 can promote the occurrence and development of tumors by regulating EMT. In the process of EMT mediated by YB1, various transcription factors and signal pathways play important roles.

Key words:Yboxbinding protein 1,Cell transformation, neoplastic,Transcription factors,Signal transduction

严雪冰, 朱庆超, 金志明. Y盒结合蛋白1与上皮-间质转化[J]. 国际肿瘤学杂志, 2013, 40(12): 896-899.

YAN Xue-Bing, ZHU Qing-Chao, JIN Zhi-Ming. Y-box-binding protein 1 and epithelialmesenchymal transition[J]. Journal of International Oncology, 2013, 40(12): 896-899.

参考文献

［1］ Eliseeva IA, Kim ER, Guryanov SG, et al. Yboxbinding protein 1 (YB1) and its functions. Biochemistry (Mosc), 2011, 76(13): 14021433. ［2］ Lasham A, Samuel W, Cao H, et al. YB1, the E2F pathway, and regulation of tumor cell growth. J Natl Cancer Inst, 2012, 104(2): 133146. ［3］ Lasham A, Moloney S, Hale T, et al. The Yboxbinding protein, YB1, is a potential negative regulator of the p53 tumor suppressor. J Biol Chem, 2003, 278(37): 3551635523. ［4］ Takahashi M, Shimajiri S, Izumi H, et al. Ybox binding protein1 is a novel molecular target for tumor vessels. Cancer Sci, 2010, 101(6): 13671373. ［5］ Astanehe A, Finkbeiner MR, Hojabrpour P, et al. The transcriptional induction of PIK3CA in tumor cells is dependent on the oncoprotein Ybox binding protein1. Oncogene, 2009, 28(25): 24062418. ［6］ Schittek B, Psenner K, Sauer B, et al. The increased expression of Y boxbinding protein 1 in melanoma stimulates proliferation and tumor invasion, antagonizes apoptosis and enhances chemoresistance. Int J Cancer, 2007, 120(10): 21102118. ［7］ Onder TT, Gupta PB, Mani SA, et al. Loss of Ecadherin promotes metastasis via multiple downstream transcriptional pathways. Cancer Res, 2008, 68(10): 36453654. ［8］ SánchezTilló E, Liu Y, de Barrios O, et al. EMTactivating transcription factors in cancer: beyond EMT and tumor invasiveness. Cell Mol Life Sci, 2012, 69(20): 34293456. ［9］ Kroepil F, Fluegen G, Vallbhmer D, et al. Snail1 expression in colorectal cancer and its correlation with clinical and pathological parameters. BMC Cancer, 2013, 13: 145. ［10］ Evdokimova V, Tognon C, Ng T, et al. Translational activation of snail1 and other developmentally regulated transcription factors by YB1 promotes an epithelialmesenchymal transition. Cancer Cell, 2009, 15(5): 402415. ［11］ Fu J, Qin L, He T, et al. The TWIST/Mi2/NuRD protein complex and its essential role in cancer metastasis. Cell Res, 2011, 21(2): 275289. ［12］ Yang F, Sun L, Li Q, et al. SET8 promotes epithelialmesenchymal transition and confers TWIST dual transcriptional activities. EMBO J, 2012, 31(1): 110123. ［13］ Shiota M, Yokomizo A, Itsumi M, et al. Twist1 and Yboxbinding protein1 promote malignant potential in bladder cancer cells. BJU Int, 2011, 108(2 Pt 2): E142149. ［14］ Song YH, Shiota M, Yokomizo A, et al. Twist1 and Yboxbinding protein1 are potential prognostic factors in bladder cancer. Urol Oncol, 2013, In press. ［15］ Jürchott K, Kuban RJ, Krech T, et al. Identification of Ybox binding protein 1 as a core regulator of MEK/ERK pathwaydependent gene signatures in colorectal cancer cells. PLoS Genet, 2010, 6(12): e1001231. ［16］ Toulany M, Schickfluss TA, Eicheler W, et al. Impact of oncogenic KRAS on YB1 phosphorylation induced by ionizing radiation. Breast Cancer Res, 2011, 13(2): R28. ［17］ Sinnberg T, Sauer B, Holm P, et al. MAPK and PI3K/AKT mediated YB1 activation promotes melanoma cell proliferation which is counteracted by an autoregulatory loop. Exp Dermatol, 2012, 21(4): 265270. ［18］ Lyabin DN, Eliseeva IA, Ovchinnikov LP. YB1 synthesis is regulated by mTOR signaling pathway. PLoS One, 2012, 7(12): e52527. ［19］ Rauen T, Raffetseder U, Frye BC, et al. YB1 acts as a ligand for Notch3 receptors and modulates receptor activation. J Biol Chem, 2009, 284(39): 2692826940. ［20］ Lee C, Dhillon J, Wang MY, et al. Targeting YB1 in HER2 overexpressing breast cancer cells induces apoptosis via the mTOR/STAT3 pathway and suppresses tumor growth in mice. Cancer Res, 2008, 68(21): 86618666. ［21］ Takeuchi A, Shiota M, Tatsugami K, et al. YB1 suppression induces STAT3 proteolysis and sensitizes renal cancer to interferonα. Cancer Immunol Immunother, 2013, 62(3): 517527. ［22］ Fraser DJ, Phillips AO, Zhang X, et al. Ybox protein1 controls transforming growth factorβ1 translation in proximal tubular cells. Kidney Int, 2008, 73(6): 724732. ［23］ Higashi K, Inagaki Y, Fujimori K, et al. Interferongamma interferes with transforming growth factorbeta signaling through direct interaction of YB1 with Smad3. J Biol Chem, 2003, 278(44): 4347043479. ［24］ Bader AG, Felts KA, Jiang N, et al. Y boxbinding protein 1 induces resistance to oncogenic transformation by the phosphatidylinositol 3kinase pathway. Proc Natl Acad Sci USA, 2003, 100(21): 1238412389. ［25］ Evdokimova V, Tognon C, Ng T, et al. Reduced proliferation and enhanced migration: two sides of the same coin? Molecular mechanisms of metastatic progression by YB1. Cell Cycle, 2009, 8(18): 29012906.

[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.

Y-box-binding protein 1 and epithelialmesenchymal transition

PDF

可视化

被引次数

摘要/Abstract

引用本文

使用本文

参考文献

相关文章15

编辑推荐

Metrics

本文评价