目的 研究磷脂酰肌醇3-激酶（PI3K）和磷酸化蛋白激酶B（p-Akt）在人膀胱尿路上皮癌組織中的表達(dá)特征及臨床意義。 方法 2005年6月－2010年7月，采用免疫組織化學(xué)法檢測40例膀胱尿路上皮癌組織及10例正常膀胱組織PI3K與p-Akt的表達(dá)，并對結(jié)果進行統(tǒng)計學(xué)分析。 結(jié)果 PI3K和p-Akt在正常膀胱黏膜組織陽性表達(dá)率均低于膀胱尿路上皮癌組織中，差異均有統(tǒng)計學(xué)意義（P＜0.05）。同一標(biāo)本中PI3K和p-Akt的表達(dá)不具有相關(guān)性（r=0.051，P=0.747）。 結(jié)論 PI3K、p-Akt在膀胱尿路上皮癌中高表達(dá)，兩者在膀胱尿路上皮癌中共同促其發(fā)展，但其在膀胱尿路上皮癌的預(yù)后和進展中的作用尚不明確。
引用本文： 潘衛(wèi)兵,朱斌,金巖,謝禮仁,楊凱鈞. 磷脂酰肌醇3-激酶和磷酸化蛋白激酶B在膀胱尿路上皮癌中的表達(dá)及意義. 華西醫(yī)學(xué), 2012, 27(4): 501-503. doi: 復(fù)制
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| 10. | Hanada M, Feng J, Hemmings BA. Structure, regulation and function of PKB/AKT--a major therapeutic target[J]. Biochim Biophys Acta, 2004, 1697(1-2): 3-16. |
| 11. | Eblin KE, Bredfeldt TG, Buffington S, et al. Mitogenic signal transduction caused by monomethylarsonous acid in human bladder cells: role in arsenic-induced carcinogenesis[J]. Toxicol Sci, 2007, 95(2): 321-330. |
| 12. | Qiao M, Sheng S, Pardee AB. Metastasis and AKT activation[J]. Cell Cycle, 2008, 7(19): 2991-2996. |
| 13. | Coffer PJ, Jin J, Woodgett JR. Protein kinase B (c-Akt): a multifunctional mediator of phosphatidylinositol 3-kinase activation[J]. Biochem J, 1998, 335( Pt 1): 1-13. |
| 14. | Song G, Ouyang GL, Bao SD. The activation of Akt/PKB signaling pathway and cell survival[J]. J Cell Mol Med, 2005, 9(1): 59-71. |
| 15. | 費洪榮, 王鳳澤. PI3K/Akt信號通路的調(diào)控與腫瘤血管生成[J]. 生命的化學(xué), 2010, 30(1): 38-41. |
- 1. Hartmann W, Digon-Söntgerath B, Koch A, et al. Phosphatidylinositol 3’-kinase/AKT signaling is activated in medulloblastoma cell proliferation and is associated with reduced expression of PTEN[J]. Clin Cancer Res, 2006, 12(10): 3019-3027.
- 2. Nyåkern M, Tazzari PL, Finelli C, et al. Frequent elevation of Akt kinase phosphorylation in blood marrow and peripheral blood mononuclear cells from high-risk myelodysplastic syndrome patients[J]. Leukemia, 2006, 20(2): 230-238.
- 3. Gao N, Flynn DC, Zhang Z, et al. G1 cell cycle progression and the expression of G1 cyclins are regulated by PI3K/AKT/mTOR/p70S6K1 signaling in human ovarian cancer cells[J]. Am J Physiol Cell Physiol, 2004, 287(2): C281-C291.
- 4. Chang F, Lee JT, Navolanic PM, et al. Involvement of PI3K/Akt pathway in cell cycle progression, apoptosis, and neoplastic transformation: a target for cancer chemotherapy[J]. Leukemia, 2003, 17(3): 590-603.
- 5. Skinner HD, Zheng JZ, Fang J, et al. Vascular endothelial growth factor transcriptional activation is mediated by hypoxia-inducible factor 1alpha, HDM2, and p70S6K1 in response to phosphatidylinositol 3-kinase/AKT signaling[J]. Biol Chem, 2004, 279(44): 45643-45651.
- 6. Jiang BH, Liu LZ. AKT signaling in regulating angiogenesis[J]. Curr Cancer Drug Targets, 2008, 8(1): 19-26.
- 7. Engelman JA. Targeting PI3K signalling in cancer: opportunities, challenges and limitations[J]. Nat Rev Cancer, 2009, 9(8): 550-562.
- 8. Martelli AM, Tabellini G, Borgatti P, et al. Nuclear lipids: new functions for old molecules?[J]. J Cell Biochem, 2003, 88(3): 455-461.
- 9. Vanhaesebroeck B, Leevers SJ, Ahmadi K, et al. Synthesis and function of 3-phosphorylated inositol lipids[J]. Annu Rev Biochem, 2001, 70(11): 535-602.
- 10. Hanada M, Feng J, Hemmings BA. Structure, regulation and function of PKB/AKT--a major therapeutic target[J]. Biochim Biophys Acta, 2004, 1697(1-2): 3-16.
- 11. Eblin KE, Bredfeldt TG, Buffington S, et al. Mitogenic signal transduction caused by monomethylarsonous acid in human bladder cells: role in arsenic-induced carcinogenesis[J]. Toxicol Sci, 2007, 95(2): 321-330.
- 12. Qiao M, Sheng S, Pardee AB. Metastasis and AKT activation[J]. Cell Cycle, 2008, 7(19): 2991-2996.
- 13. Coffer PJ, Jin J, Woodgett JR. Protein kinase B (c-Akt): a multifunctional mediator of phosphatidylinositol 3-kinase activation[J]. Biochem J, 1998, 335( Pt 1): 1-13.
- 14. Song G, Ouyang GL, Bao SD. The activation of Akt/PKB signaling pathway and cell survival[J]. J Cell Mol Med, 2005, 9(1): 59-71.
- 15. 費洪榮, 王鳳澤. PI3K/Akt信號通路的調(diào)控與腫瘤血管生成[J]. 生命的化學(xué), 2010, 30(1): 38-41.