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为探讨癌细胞淋巴管侵润转移机理，对8例直肠腺癌患者的癌周组织和转移淋巴结，以及5例正常人的直肠组织和淋巴结，采用免疫组织化学方法，检测细胞间细胞粘附分子（ICAM－1）和核转录因子KBp65（NFKBp65）的表达。同时通过地高辛碱性磷酸酶标记的寡核苷酸探针，利用原位杂交技术，对8例直肠腺癌患者的癌周组织和转移淋巴结以及5例正常人的直肠组织和淋巴结，进行ICAM－1基因的NFKB结合位点的检测。结果显示：直肠腺癌病人转移的淋巴结和癌周直肠组织中的淋巴管内皮细胞都有ICAM－1和NFKBp65表达，而在正常人的淋巴管内皮细胞无ICAM－1和NFKBp65的表达；直肠腺癌病人转移淋巴结和癌周直肠组织中的淋巴管内皮细胞核内ICAM１的启动子中存在有NFKB 结合位点。提示ICAM－1的转录，取决于可诱导的NFKB 蛋白质复合物与ICAM－1的NFKB部位结合，阻碍NFKB因子的活化能够防止癌细胞的淋巴管转移。
To investigate the mechanism of lymphatic invasion and metastasis of cancer cells, 8 cases of rectal adenocarcinoma tissues and metastatic lymph nodes, and 5 cases of normal human rectal tissues and lymph nodes were examined by immunohistochemistry to detect intercellular adhesion molecules. Expression of (ICAM-1) and nuclear transcription factor KBp65 (NFKBp65). At the same time, digoxin alkaline phosphatase labeled oligonucleotide probes were used to perform in situ hybridization in 8 cases of rectal adenocarcinoma tissues and metastatic lymph nodes as well as 5 cases of normal human rectal tissues and lymph nodes. ICAM-1 gene NFKB binding site detection. The results showed that the lymphatic endothelium in metastatic lymph nodes and pericancerous rectal tissue of patients with rectal adenocarcinoma had ICAM-1 and NFKBp65 expression, but there was no expression of ICAM-1 and NFKBp65 in normal human lymphatic endothelial cells; rectal glands There is a NFKB binding site in the promoter of ICAM1 in the nucleus of lymphatic endothelial cells in metastatic lymph nodes and pericancerous rectal tissue of cancer patients. It suggests that the transcription of ICAM-1 depends on the inducible binding of NFKB protein complexes to the NFKB site of ICAM-1, and that blocking the activation of NFKB factors can prevent the lymphatic metastasis of cancer cells.