期刊文献+

mTOR/P70S6K信号通路在小儿血管瘤演变中的作用 被引量:10

The role of mTOR/p70S6K signaling pathway in the development of hemangioma of children
原文传递
导出
摘要 目的 探讨mTOR/p70S6K信号通路在小儿血管瘤的发生、发展及消退过程中的作用.方法 收集未经其他治疗、单纯手术切除并经病理诊断为血管瘤的标本31例,结合Mulliken分类法与增殖细胞核抗原(PCNA)表达对血管瘤进行分类和分期,免疫组织化学检测并比较增生期血管瘤和消退期血管瘤组织中雷帕霉素靶蛋白(mTOR)和p70S6K-a的表达水平.结果 18例增殖期血管瘤mTOR、p70S6K-a的积分光密度分别为6336.47±1655.89,588.72±223.87;13例消退期血管瘤mTOR、p70S6K-a的积分光密度分别为846.22±297.09,3235.64±947.86;血管瘤增殖期p70S6K-a的积分光密度明显低于消退期,差异有统计学意义(P<0.01).血管瘤增殖期mTOR的积分光密度明显高于消退期,差异有统计学意义(P<0.01).结论 小儿血管瘤组织中有mTOR、p70S6K-α表达,mTOR/p70S6K信号通路可能在小儿血管瘤的病理演变中发挥作用. Objective To investigate the role of mTOR/p70S6K signaling pathway in the development of hemangioma in children. Methods Hemangioma specimens from 31 patients without any other treatment except surgery were classified by Mulliken's classification. The expression of proliferating cell nuclear antigen (PCNA), mammalian target of rapamycin (mTOR) and p70 ribosomal S6-kinase (p70S6K-α) were detected with immunohistochemistry. Results Eighteen cases of hemagioma specimens were classified as in proliferating phase, 13 as in involuting phase. For hemangiomas in proliferating phase, the IOD of mTOR and p70S6K-α were 6336. 47 ± 1655. 89 and 588. 72 ± 223. 87 respectively, while for hemagiomas in the involuting phase, the IOD of mTOR and p70S6K-α were 846. 22± 297. 09 and 3235. 64 ± 947. 86 respectively. IOD of p70S6K-α in hemangiomas in the involving phase was significantly higher than that in the proliferating phase (P<0. 01 ). IOD of mTOR in the hemagiomas in proliferating phase was significantly higher than that in the involuting phase (P<0. 01 ). Conclusions The mTOR/p70S6K signaling pathways may play an important role in growth and development of pediatric hemangioma.
出处 《中华小儿外科杂志》 CSCD 北大核心 2010年第12期885-887,共3页 Chinese Journal of Pediatric Surgery
基金 贵州省优秀科技教育人才省长专项资金项目 [黔省专合字(2010)67号] 贵州省科技厅基金[黔科合J字(2007)2215号] 贵州省社发攻关项目[黔科合SY(2008)3028]号 遵义市重点科技计划项目培育及人才培养划项目[遵科培字(2009)04号]
关键词 血管瘤 内皮细胞 雷帕霉素结合蛋白质类 Hemangioma Endothelial cells Rapamycin binding proteins
  • 相关文献

参考文献6

二级参考文献52

  • 1夏扬,高颖,徐光,刘静.抑癌基因p53与p16及PCNA蛋白在皮肤增生期血管瘤中的表达及其对血管内皮细胞的干预[J].中国临床康复,2006,10(25):99-101. 被引量:2
  • 2俞松,刘文英,胡月光,唐耘熳,侯昉,刘鹏.Fas、bcl-2与移植血管瘤自然退化的动态研究[J].中华小儿外科杂志,2007,28(3):149-151. 被引量:7
  • 3侯桂琴,鲁照明,穆欣,刘洪涛,刘兰琦,许培荣,薛乐勋,王建人.雷帕霉素靶蛋白信号通路在食管癌细胞系中激活状态的研究[J].中国肿瘤,2007,16(4):260-262. 被引量:3
  • 4陈超,杨体泉.婴幼儿血管瘤内皮细胞凋亡研究进展[J].实用儿科临床杂志,2007,22(11):869-871. 被引量:9
  • 5Razon MJ, Kraling BM, Mulliken JB, et al. Increased apoptosis coincides with onset of involution in infantile hemangioma. Mircocirculation, 1998,5 : 189-195.
  • 6Muzio M, Chinnaiyan AM, Kischkei FC, et al. FLICE, a novel FADD homologous ICE/CED-3-1ike protease, is recruited to the CD95 (Fas/Apol) death inducing signaling complex (DISC). Cell, 1996,85 : 817-827.
  • 7Maedler K, Fontana A, Ris F, et al. FLIP switches Fasmediated glucose signaling in human pancreatic β cells from apoptosis to cell replication. Proc Natl Acad Sci USA, 2002, 99:8236-8241.
  • 8Kim Y, Suh N, Sporn M,et al. An inducible pathway for degradation of FLIP protein sensitizestumor eellsto TRAIL-induced apoptosis. J Biol Chem,2002,277: 22320- 22329.
  • 9Rescigno M, Piguet V, Valzasina B, et al. Fas engagement induces the maturation of dendritic cells (DCs), the release of interleukin (IL)-beta, and the production of interferon gamma in the absence of IL-12 during DC-Tcell cognate interaction: a new role for fas ligand in inflammatory responses. J Exp Med,2000, 192:1661-1668.
  • 10Kataoka T, Budd RC. The caspase-8 inhibitor FLIP promotes actievation of NF-kappB and Erk signaling pathways. Curt Biol, 2000,10 : 640-648.

共引文献34

同被引文献118

  • 1Liu JF, Zhou XK, Chen JH, Yi G, Chen HG, Ba MC, Lin SQ, Qi YC..Up-regulation of PIK3CA promotes metastasis in gastric carcinoma[J].World Journal of Gastroenterology,2010,16(39):4986-4991. 被引量:21
  • 2俞松,刘文英,唐耘熳,魏艇.血管瘤裸鼠移植模型生物学特性的动态观察[J].中华小儿外科杂志,2005,26(5):264-267. 被引量:10
  • 3Sugatani T,Hruska KA.Akt1/Akt2 and mammalian target of rapamycin/Bim play critical roles in osteoclast differentiation and survival,respectively,whereas Akt is dispensable for cell survival in isolated osteoclast precursors.J Biol Chem,2005,280(5):3583-3589.
  • 4Inoki K,Li Y,Zhu T,et al.TSC2 is phosphorylated and inhibited by Akt and suppresses Mtor signalling Nat Cell Biol,2002,4(9):648-657.
  • 5Amin RM,Hiroshima K,Miyagi Y,et al.Role of the pI3K/Akt,mTOR,and STK11/LKB1 pathways in the tumorigenesis of sclerosing hemangioma of the lung.Pathol Int,2008,58(1):38-44.
  • 6Su JC,Lin KL, Chien CM, et al. Naphtho [-1,2-b] furan-4,5- dion inactivates EGFR and PI3K/Akt signaling pathways in human lung adenocarcinoma A549 cells. Life SCI, 2010, 86 (5- 6) : 207-213.
  • 7Skeen J E, Bhaskar PT, Chen CC, et al. Akt deficiency in pairs normal cell proliferation and suppresses on congenesis in a p53-independent and mTorCl-dependentm anner. Cancer Cell, 2006,10(4) : 269-280.
  • 8Pu P, Kang C, Zhang Z, et al. Downregulation of pI3KCB by siRNA suppres malignant glima cell growth in vitro and in vivo. Technol Cancer Res Treat, 2006,5 (3) : 271-280.
  • 9Engelman JA, Luo J, Cantley LC. The evolution of phosphati- dylinositol 3-kinases Asregulatons of growth and metabolism. Nat Rev Genet,2006,7(8):606 619.
  • 10Chun KH,Kosmeder JW 2nd, Sun S, et al. Effects of deguelin on the phosphatidy linositol 3-kinase/Akt pathway and apopto- sis in premalig nant human bronchial epithelial cells. J Natl Cancer Inst, 2003,95 (4) : 291-302.

引证文献10

二级引证文献60

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部