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尖锐湿疣患者皮损中SOCS1和PIAS1的表达及意义 被引量:11

Expression and significance of suppressor of cytokine signaling-1 and protein inhibitor of activated STAT-1 in condyloma acuminatum
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摘要 目的探讨尖锐湿疣(CA)皮损角质形成细胞中细胞因子信号转导JAK/STAT通路负调控蛋白细胞因子信号抑制剂-1(SOCS1)和活化STAT的蛋白抑制剂-1(PIAS1)的表达。方法采用SP免疫组化染色技术检测40例CA患者皮损、20例宫颈癌和20例正常人皮肤(包皮)中SOCS1和PIAS1的表达及分布。结果①CA患者皮损中SOCS1和PIAS1的表达阳性细胞分布主要位于棘细胞层,为棕黄着色,阳性反应定位胞质;宫颈鳞状细胞癌亦为胞质阳性表达,棕黄着色,呈弥漫性分布;而正常包皮少数阳性着色主要定位于基底层细胞的胞质,呈浅黄着色。②CA皮损中SOCS1和PIAS1的表达阳性率分别为85%和80%,高于在正常人上皮中的表达(阳性率分别为30%和35%),两组比较差异均有统计学意义(前者X^2=18.15,P〈0.01;后者X^2=11.87,P〈0.01);宫颈癌中SOCS1和PIAS1的表达阳性率分别为90%和85%,虽较CA有升高,但两者比较差异均无统计学意义(两者均P〉0.05)。③CA中SOCS1与PIAS1的表达无显著相关性(rs=0.14,P〉0.05)。结论CA皮损中可能通过细胞因子信号转导负调控蛋白SOCS1和PIAS1在角质形成细胞过度增殖或恶性转化过程中起调控作用。 Objective To explore the expression of suppressor of cytokine signaling-1 ( SOCS1 ) and protein inhibitor of activated STAT-1 ( PIAS1 ) in keratinocytes of condyloma acuminatum ( CA ) lesions and its significance. Methods SP immunohistochemistry technique was used to detect the expression and distribution of SOCS1 and PIAS1 in lesions from 40 cases of CA and 20 cases of cervical cancer, and in skin (foreskins) of 20 normal controls. Results In CA lesions, SOCS1 and PIAS1 were stained brown-yellow in the cytoplasm of keratinocytes, and positive cells were mainly distributed in the prickle layer. In cervical cancer, they were also stained brown-yellow and diffusely distributed in the cytoplasm of carcinoma cells. In normal skin, SOCS1 and PIAS1 weakly expressed in the cytoplasm of keratinocytes in basal layer, and were stained pale yellow. The positive rates of both SOCS1 and PIAS1 were significantly higher in CA lesions than in normal skin (85% vs 30%, X^2 = 18.15, P 〈 0.01; 80% vs 35%, X^2 = 11.87, P 〈 0.01 ). Although the positive rates of SOCS1 ( 90% ) and PIAS1 ( 85% ) in cervical cancer were higher than those in CA, no significant difference was found between them ( both P 〉 0.05 ). There was no significant correlation between the expression.of SOCS 1 and PIASI in CA lesions ( rs = 0.14, P 〉 0.05 ). Conclusion SOCS1 and PIAS1 may play a role in the overproliferation and malignant transformation of keratinocytes in CA lesions.
出处 《中华皮肤科杂志》 CAS CSCD 北大核心 2007年第5期283-285,共3页 Chinese Journal of Dermatology
基金 浙江省卫生厅资助课题(2005A06)
关键词 尖锐湿疣 SOCS1 PIAS1 Condylomata acuminata SOCSI PIASI
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参考文献8

  • 1Yoshida T, Ogata H, Kamio M, et al. SOCS1 is a suppressor of liver fibrosis and hepatitis-induced carcinogenesis. J Exp Med, 2004, 199(12): 1701-1707.
  • 2陶小华,董玉娥,孟群,潘卫利,程浩.Stat1和含SH2区域的SHP-1在尖锐湿疣中的表达[J].中华皮肤科杂志,2006,39(9):515-517. 被引量:2
  • 3李圆圆,王玉坤,郝宝珍.尖锐湿疣、鲍恩样丘疹病、Bowen病及外阴鳞状细胞癌皮损中端粒酶的表达[J].中华皮肤科杂志,2006,39(5):266-268. 被引量:5
  • 4Ilangumaran S, Rottapel R. Regulation of cytokine receptor signaling by SOCS1. Immunol Rev, 2003, 192(1): 196-211.
  • 5Kamio M, Yoshida T, Ogata H, et al. SOCS1 [corrected] inhibits HPV-E7-mediated transformation by inducing degradation of E7 protein. Oncogene, 2004, 23 ( 17): 3107-3115.
  • 6Ungureanu D, Vanhatupa S, Kotaja N, et al. PIAS proteins promote SUMO-1 conjugation to STAT1. Blood, 2003, 102 (9): 3311-3313.
  • 7Rosas-Acosta G, Langereis MA, Deyrieux A, et al. Proteins of the PIAS family enhance the sumoylation of the papillomavirus E1 protein. Virology, 2005, 331 ( 1 ):190-203.
  • 8Megidish T, Xu JH, Xu CW. Activation of p53 by protein inhibitor of activated Statl (PIAS1). J Biol Chem, 2002, 277 (10): 8255-8259.

二级参考文献16

  • 1董玉娥,沈建根,朱永良,潘卫利,孟群.含c-Src同源序列SH2酪氨酸磷酸酶在尖锐湿疣组织中的表达[J].中华皮肤科杂志,2004,37(7):400-402. 被引量:2
  • 2苏明,程浩,盛彩霞,吴能定,李凌,项力俭,李雅芬,钟剑波.尖锐湿疣患者角质形成细胞中活化型细胞外信号调控蛋白激酶和活化型p38的检测[J].中华皮肤科杂志,2004,37(10):569-571. 被引量:8
  • 3Yu DS,Kim G,Song HJ,et al.Morphometric assessment of nuclei in Bowen's disease and bowenoid papulosis.Skin Res Technol,2004,10:67-70.
  • 4Chen Z,Smith K J,Skelton HG 3rd,et al.Telomerase activity in Kaposi's sarcoma,squamous cell carcinoma,and basal cell carcinoma.Exp Biol Med(Maywood),2001,226:753-757.
  • 5Wu A,Ichihashi M,Ueda M.Correlation of the expression of human telomerase subunits with telomerase activity in normal skin and skin tumors.Cancer,1999,86:2038-2044.
  • 6Villa R,Porta CD,Folini M,et al.Possible regulation of telomerase activity by transcription and alternative splicing of telomerase reverse transcriptase in human melanoma.J Invest Dermatol,2001,116:867-873.
  • 7Zhang Y,He DM.Effect of antisense hTERT mRNA oligodeoxynucleotide on telomerase activity of leukemic cells.Cell Biol Int,2002,26:427-431.
  • 8Park HR,Min SK,Cho HD,et al.Expression profiles of p63,p53,survivin,and hTERT in skin tumors.J Cutan Pathol,2004,31:544-549.
  • 9Parris CN,Jezzard S,Silver A,et al.Telomerase activity in melanoma and non-melanoma skin cancer.Br J Cancer,1999,79:47-53.
  • 10Bowman T,Garcia R,Turkson J,et al.STATs in oncogenesis.Oncogene,2000,19:2474-2488.

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