摘要
目的研究蛋白激酶C(PKC)、粘附分子CD44变构体CD44V3-10在非小细胞性肺癌(NSCLC)中定量表达及在肺癌发生及转移中的作用。方法根据放射免疫结合法,用[r-32P]标记的ATP掺入外源性底物测定PKC的活性;应用免疫组织化学Envision二步染色法测定肺癌组织CD44V3-10的表达。结果肺癌组织细胞胞膜及胞浆中PKC活性分别为(4.56±0.27)nmol/(mg·pr/min),(2.01±0.12)nmol/(mg·pr/min),显著高于正常肺组织(P<0.01)。低分化、未分化肺癌的PKC总活性分别为(6.72±0.14)nmol/(mg·pr·/min)、(6.98±0.17)nmol/(mg·pr/min);CD443-10定量表达IOD值分别为(368.2±25.4)、(389.8±24.8),都显著高于高分化、中分化肺癌(P<0.01);有转移肺癌PKC总活性(6.86±0.15)nmol/(mg·pr/min)、CD44V3-10定量表达IOD值(387.6±25.6)都显著高于无转移肺癌(P<0.01)。结论肺癌组织中存在PKC异常活化现象;PKC活化上调了CD44V3-10的表达,共同促进了肺癌的发生及转移。
[Objective]To investigate the quantitative expression and roles of protein kinase C (PKC), Variant CD44 (CD44V3-10) adhesion molecules in Non-small cellular lung cancer (NSCLC). PKC activity was assayed by measuring the incorporation of 32P from ATP into protamine. CD44V3-10 was detected by tne immunohistochemical Envision technigue. The membranous and cytosolic PKC activity in NSCLC were (4.56±0.27) nmol/(mg·pr/min), (2.01±0.12) nmol/(mg·pr/min) respectively, which were all significantly higher than that in normal lung tissues( P <0.01). The total PKC activity and IOD of CD44V3-10 in low or non-differentiated lung cancer cells were (6.72±0.14) nmol/(mg·pr/min), (6.98±0.17) nmol/(mg·pr/min), (368.2±25.4) and (389.8±24.8) respectively, which were all prominently higher than higher class cells, P <0.01. The total PKC activity (6.86±0.15)nmol/(mg·pr/min) and IOD of CD44V3-10 (387.6±25.6) in metastatic lung cancer were all remarkably higher than that in non-metastatic class cells, P <0.01. [Conclusions] PKC activation exists in lung cancer cells, which up-regulates the expression of CD44V3-10, and they all promotes the development and metastasis of lung cancer cells.
出处
《中国现代医学杂志》
CAS
CSCD
北大核心
2005年第8期1158-1160,共3页
China Journal of Modern Medicine
