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胰腺癌中CIP2A、PI3K和Survivin的表达及临床意义 被引量:4

Expression and clinical significance of CIP2A, PI3K, and survivin in pancreatic carcinomas
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摘要 目的 研究胰腺癌组织中蛋白磷酸酶2A癌性抑制因子(CIP2A)、磷脂酰肌醇3-激酶(PI3K)及Survivin的表达及其临床意义.方法 采用免疫组织化学法检测64例胰腺癌组织及癌旁组织中CIP2A、PI3K及Survivin的表达情况,并分析它们与临床病理参数的关系.结果 CIP2A在胰腺癌组织及癌旁组织中的阳性表达率分别为70.3%,5.6%;PI3K在胰腺癌组织及癌旁组织中的阳性表达率分别为73.4%,8.3%;Survivin在胰腺癌组织及癌旁组织中的阳性表达率分别为75.0%,2.8%,差异均有统计学意义(P<0.05).CIP2A、PI3K及Survivin在胰腺癌组织中的表达均与肿瘤分化程度、TNM分期、神经浸润及淋巴结转移有关(均P<0.05);经Spearman等级相关性分析,CIP2A与PI3K及Survivin在胰腺癌组织中的表达均呈正相关(均P<0.05).PI3K与Survivin在胰腺癌组织中的表达也呈正相关(P<0.05).结论 CIP2A参与了胰腺癌恶性进展,可能通过激活PI3K/蛋白激酶B(Akt)/Survivin信号通路促进胰腺癌发生、侵袭和转移.CIP2A有望成为治疗胰腺癌的一个靶向治疗基因. Objective To investigate the expressions of cancerous inhibitor of protein phosphatase2A (CIP2A),phosphatidylinositol 3-kinase(PI3K),and survivin in pancreatic carcinomas and their clinical significance.Methods The expressions of CIP2A,PI3K,and survivin proteins were tested by immunohistochemistry in 64 cases of pancreatic carcinomas and adjacent paracancerous tissues.Results The positive rate of CIP2A in pancreatic carcinomas was significantly higher than adjacent paracancerous tissues (70.3% vs 5.6%,P 〈0.05).Significant difference was observed in the expression rate of PI3K between the patients with pancreatic carcinomas and paracancerous tissues (73.4% vs 8.3%,P 〈0.05).Significant difference was also observed in the expression rate of survivin between the patients with pancreatic carcinomas and paracancerous tissues (75.0% vs 2.8%,P 〈0.05).CIP2A,PI3K,and survivin were significantly differentially expressed in pancreatic carcinoma among different tumor differentiation,tumor node metastasis (TNM) stage,and neural invasion and lymph node metastasis (all P 〈 0.05).Spearman correlation analysis showed significantly positive correlation between the expressions of CIP2A and the others (PI3K and survivin) (both P 〈0.05),and between the expressions of PI3K and surviving (P 〈0.05).Conclusions CIP2A was involved in the development of pancreatic carcinomas and might activate the PI3K/Akt/survivin pathway.Our data identified CIP2A as a critical oncoprotein involved in cell proliferation,invasion,and metastasis.It could serve as a therapeutic target for pancreatic carcinomas.
出处 《中国医师杂志》 CAS 2015年第2期198-201,共4页 Journal of Chinese Physician
关键词 胰腺肿瘤/代谢 蛋白质磷酸酶2/代谢 肿瘤抑制蛋白质类/代谢 1-磷脂酰肌醇3-激酶/代谢 微管相关蛋白质类/代谢 Pancreatic neoplasms/ME Protein phosphatase 2/ME Tumor suppressor proteins/ME 1-phosphatidylinositol 3-kinase/ME Microtubule-associated proteins/ME
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  • 1Riall TS, Cameron JL, Lillemoe KD, et al. Resected periampul- lary adenocareinoma: 5-year survivors and their 6- to 10-year fol- low-up. Surgery,2006,140(5 ) :764-772.
  • 2Kim RD, Kundhal PS, McGilvray ID, et al. Predictors of failure after pancreaticoduodenectomy for ampullary carcinoma. J Am Coil Surg ,2006, 202 ( 1 ) : 112-119.
  • 3Shin S, Sung BI, Chao YS, et al. An anti-apoptotie protein human- survivin is a direct inhibitor of caspase-2 and-7. Bio Chemistry,2001,40(4) :1117-1123.
  • 4Ambrosini G, Adida C, Altieri DC. A novel anti-apoptosis gene, survivin,expressed in cancer and lymphoma. Nat Med, 1997,3 (8) :917-921.
  • 5Langlois MJ, Bergeron S, Bernatchez G, et al. The PTEN phos- phatase controls intestinal epithelial cell polarity and barrier func- tion: role in colorectal cancer progression. Plos One, 2010,5 (12) : e15742.
  • 6Wang Y, Romigh T, He X, et al. Resveratrol regulates the PTEN/AKT pathway through androgen receptor-dependent and independent mechanisms in prostate cancer cell lines. Hum Mol Genet,2010,19 ( 22 ) : 4319-4329.
  • 7Kalliakmanis JG, Kouvidou Ch, Latoufis C, et al. Survivin expres- sion in colorectal carcinomas: correlations with clinicopathological parameters and survival. Dig Dis Sci ,2010,55 (10) :2958-2964.
  • 8Sarela AI, Verbeke CS, Ramsdale J, et al. Expression of Sur- vivin, a novel inhibitor of apoptosis and cell cycle regulatory pro- tein, in pancreatic adenocarcinoma. British Journal of Cancer, 2002,86(6) :886-892.
  • 9Santini D, Vincenzi B, Tonini G, et al. Cyclooxygenase-2 over- expression is associated with a poor outcome in resected ampullary cancer patients. Clin Cancer Res,2005,11 (10) :3784-3789.
  • 10Carter BZ, Milella M, Ahieri DC, el al. Cytokine-regulated expres- sion of surviving in myeloid leukemia. Blood,2001,97 (9) :2784- 2790.

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  • 1Sun M, Trinh QD. Diagnosis and Staging of Bladder Cancer[ J]. Hematol Oncol Clin North Am,2015,29(2) :205-218.
  • 2Malats N, Real FX. Epidemiology of Bladder Cancer[ J]. Hema-tol Oneol Clin North Am,2015,29(2) :177-189.
  • 3Martin-Doyle W, Kwiatkowski D J. Molecular Biology of Bladder Cancer[J]. Hematol Oncol Clin North Am, 2015,29 ( 2 ) : 191 - 203.
  • 4Han H, Yi F. New insights into TRP channels: Interaction with pattern recognition receptors [ J]. Channels ( Austin ) , 2013,8 ( 1 ) :257-260.
  • 5Farfariello V, Iamshanova O, Germain E, et al. Calcium homeo- stasis in cancer: A focus on senescence[ J]. Biochim Biophys Ac- ta,2015,18 (3) :362-365.
  • 6Wang Y, Yang Z, Meng Z, et at. Knockdown of TRPM8 suppresses cancer malignancy and enhances epirubicin-induced apoptosis in human osteosarcoma ceils [ J ]. Int J Biol Sci, 2013,10 ( 1 ) : 90- 102.
  • 7Liu J, Chen Y, Shuai S, et al. TRPM8 promotes aggressiveness of breast cancer cells by regulating EMT via activating AKT/GSK- 3 beta pathway [ J ]. Tumour Biol,2014,35 ( 9 ) : 8969-8977.
  • 8Yu S, Xu Z, Zou C, et al. Ion channel TRPM8 promotes hypoxic growth of prostate cancer cells via an 02 -independent and RACKl-mediated mechanism of HIF-lalpha stabilization [ J ]. J Patho1,2014,234 ( 4 ) :514-525.
  • 9Du GJ, Li JH, Liu WJ, et al. The combination of TRPM8 and TRPA1 expression causes an invasive phenotype in lung cancer [J]. Tumour Biol,2014,35(2) :1251-1261.
  • 10Yee NS,Zhou W,Lee M. Transient receptor potential channel TR- PM8 is over-expressed and required for cellular proliferation in pancreatic adenocarcinoma[ J]. Cancer Iett ,2010,297( 1 ) :49-55.

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