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卵巢上皮性癌组织中磷酸化信号转导及转录活化因子3和Ki67蛋白的表达 被引量:2

Expression of p-signal transducers and activators of transcription3 and Ki67 in epithelial ovarian carcinoma tissue
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摘要 目的:检测卵巢上皮性癌组织中磷酸化信号转导及转录活化因子3(p-STAT3)和Ki67蛋白的表达。方法:应用免疫组织化学SP法检测35例卵巢上皮性癌组织(高分化11例,中分化12例,低分化12例;Ⅰ、Ⅱ期16例,Ⅲ、Ⅳ期19例;有淋巴结转移20例,无淋巴结转移15例)、20例良性卵巢上皮性肿瘤组织及30例正常卵巢组织中p-STAT3和Ki67蛋白的表达。结果:正常卵巢组织、良性卵巢上皮性肿瘤组织及卵巢上皮性癌组织中p-STAT3的表达水平分别为(43.20±3.18),(50.12±4.36)及(92.57±5.26),3者相比,差异有统计学意义(F=7.605,P=0.001);Ki67的表达水平分别为(7.69±1.21)、(12.53±2.62)及(16.18±5.32),3者相比,差异有统计学意义(F=3.925,P=0.029)。卵巢上皮性癌组织中p-STAT3和Ki67的表达与临床分期、分化程度及淋巴结转移有关(p-STAT3:t/F=6.921、3.865和7.763,P均<0.05;Ki67:t/F=6.917、3.870和4.021,P均<0.05)。卵巢上皮性癌组织中p-STAT3与Ki67的表达呈正相关(rS=0.563,P<0.001)。结论:卵巢上皮性癌组织中p-STAT3与Ki67的表达升高,联合检测2者对判断卵巢上皮性癌的恶性程度和预后有一定价值。 Aim : To detect the expressions of p-signal transducers and activators of transcription3 (STAT3) and Ki67 in epithelial ovarian carcinoma tissue. Methods :The expressions of p-STAT3 and Ki67 in normal ovary ( n = 30) , benign epithelial ovarian tumor( n = 20) , and epithelial ovarian carcinoma tissue( n = 35 ; 11 cases of well differentiation, 12 cases of moderate differentiation,and 12 cases of poor differentiation;16 cases of stage I and 1] ,19 cases of stage Ili and IV ;20 cases with lymph node metastasis, 15 cases without lymph node metastasis) were detected by immunohistochemistry. Resuits : There was significant difference in the expressions of p-STAT3 [ (43.20 ± 3.18 ), (50.12 ± 4.36) , and ( 92.57 ± 5.36)] and Ki67[(7.69 ±1.21),(12.53 ±2.62),and (16. 18 ±5.32)] among the three kinds of tissue(F=7.605 and 3. 925 ,P 〈 0.05 ). The expressions of p-STAT3 and Ki6? in epithelial ovarian carcinoma tissue were related with clini- cal stage ,differentiation grade, and lymph node metastasis ( p-STAT3 : t/F = 6. 921,3. 865 and 7. 763, P 〈 0.05 ; Ki67 : t/F =6. 917,3. 870 and 4. 021 ,P 〈0.05). The expressions of p-STAT3 and Ki67 in epithelial ovarian carcinoma tissue were positively correlated (rs = 0. 563, P 〈 0. 001 ). Conclusion: The expressions of p-STAT3 and Ki67 increase in epi- thelial ovarian carcinoma tissue. Combined detection of the 2 parameters is of value in predicting the malignant degree and prognosis of epithelial ovarian carcinoma.
出处 《郑州大学学报(医学版)》 CAS 北大核心 2010年第2期246-249,共4页 Journal of Zhengzhou University(Medical Sciences)
关键词 卵巢上皮性肿瘤 磷酸化信号转导及转录活化因子3 KI67 细胞增殖 epithelial ovarian neoplasm carcinoma p-STAT3 Ki67 cell proliferation
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参考文献7

  • 1Leong PL, Andrews GA, Johnson DE, et al. Targeted inhibition of Stat3 with a decoy oligonucleotide abrogates head and neck cancer cell growth[ J]. Proc Natl Acad Sci USA, 2003,100(7) :4 138.
  • 2Adams SF, Levine DA, Cadungog MG, et al. Intraepithelial T cells and tumor proliferation: impact on the benefit from surgical cytoreduction in advanced serous ovarian cancer[J]. Cancer,2009,115(13) :2 891.
  • 3Haura EB, Turkson J, Jove R. Mechanisms of disease: insights into the emerging role of signal transducers and activators of transcription in cancer [ J]. Nat Clin Pract Oncol, 2005,2(6) :315.
  • 4Mizoguchi M, Betensky RA,Batchelor TT,et al. Activation of STAT3, MAPK, and AKT in malignant astrocytic gliomas:correlation with EGFR status, tumor grade, and survival[ J]. J Neuropathol Exp Neurol,2006,65 (12) : 1 181.
  • 5Fletcher S, Drewry JA, Shahani VM,et al. Molecular disruption of oncogenic signal transducer and activator of transcription 3 (STAT3) protein[ J]. Biochem Cell Biol,2009, 87(6) :825.
  • 6Hensleigh PA, Andrews WW, Brown Z, et al. Genital herpes during pregnancy: inability to distinguish primary and recurrent infections clinically [ J ]. Obstet Gynecol, 1997,89 (6) : 891.
  • 7Schluter C, Duchrow M,Wohlenberg C, et al. The cell proliferation-associated antigen of antibody Ki-67: a very large, ubiquitous nuclear protein with numerous repeated elements,representing a new kind of cell cycle-maintaining proteins[J]. J Cell Biol,1993,123(3) :513.

同被引文献18

  • 1Huang WT, Yang SF, Wn CC, et al. Expression of signal transducer and activator of transcription 3 and suppressor of eytokine signaling 3 in urothelial carcinoma[ J]. Kaohsiung J Med Sci,2009,25(12) :640.
  • 2Ehrmann J, Strakova N, Vrzalikova K, et al. Expression of STATs and their inhibitors SOCS and PIAS in brain tumors [J]. Neoplasma,2008,55(6) :482.
  • 3Lu Y, Fukuyama S, Yoshida R, et al. Loss of SOCS3 geneexpression converts STAT3 function from anti-apoptotic to pro-apoptotie [ J]. J Biol Chem ,2006,281 (48) :36683.
  • 4Alvarez JV,Frank DA. Genome-wide analysis of STAT tar- get genes: elucidating the mechanism of STAT-mediatedoncogenesis[ J]. Cancer Biol Ther,2004,3 ( 11 ) : 1045.
  • 5Yoshimura A. Signal transduction of inflammatory cyto-kines and tumor development [ J ]. Cancer Sci, 2006,97 (6) :439.
  • 6Howard JK, Cave B J, Oksanen L J, et al. Enhanced leptin senxitivity and attenuation of diet-induced obesity in micewith haploinsufficiency of Socs3 [ J]. Nat Med, 2004, 10 (7) :734.
  • 7Hodge DR, Hurt EM, Farrar WL. The role of IL-6 and STAT3 in inflammation and cancer [ J ]. Eur J Cancer, 2005,41 (16) :2502.
  • 8He B,You L,Uematsu K,et al. SOCS-3 is frequently si- lenced by hypermethylation and suppresses cell growth in human lung cancer [ J ]. Proc Natl Acad Sci USA, 2003, 100(24) :14133.
  • 9Niwa Y, Kanda H, Shikauchi Y, et al. Methylation silencing of SOCS-3 promotes cell growth and migration by enhan- cing JAK/STAT and FAK signalings in human hepatocellu- lar carcinoma [ J ]. Oncogene, 2005,24 ( 42 ) : 6406.
  • 10Weber A, Hengge UR, Bardenbeuer W, et al. SOCS-3 is frequently methylated in head and neck squamous cell car- cinoma and its precursor lesions and causes growth inhibi- tion[ J]. Oncogene ,2005,24(44) :6699.

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