S100 calcium binding protein A8 (S100A8),a possible novel member of NF-kappa B signal pathway in laryngeal squamous cell carcinoma (LSCC),interacts with human leukocyte antigen B (HLA-B) which carries an NF-kappa B binding site within the enhancer A. The objective of this study was to explore the molecular mechanism of S100A8 in laryngeal carcinogenesis. RT-PCR,Western blotting and immuno-histochemistry staining were applied to evaluate the expression levels of IKKα,P65,REL-B,S100A8,APAF-1 and BCL-2 genes. The signal transduction passway in which S100A8 might participate was explored by RNA interference. Flow cytometry,TUNEL assay and cell invasion in vitro were used to detect the biological behavior of Hep2 cells induced by S100A8 gene. Our results showed that high expression of S100A8 was related to tumorigenesis in LSCC and negatively correlated with the degree of differentiation,indicating that S100A8 gene could inhibit apoptosis and promote metastasis in LSCC. Additionally,the suppression of S100A8 by RNA interference down-regulated BCL-2 but not APAF-1,P65 and IKKα,while,the suppression of P65 could significantly down-regulate the expression of S100A8 gene. In conclusion,S100A8 plays an important role in P65/HLA-B/S100A8/BCL-2/Caspase-9 (-3) pathway in laryngeal carcinoma.
目的探索原发性喉鳞状细胞癌及喉癌Hep-2细胞系的特征性染色体异常，认识喉癌的细胞遗传学改变与其发病机理的相关性。方法对喉癌手术新鲜标本进行改良的原代细胞培养，G显带后核型分析；应用高分辨染色体分析法对喉癌Hep-2细胞系进行核型分析；应用6号染色体涂染探针对原发性喉癌及喉癌细胞系进行分子细胞遗传学研究。结果4例原发性喉癌原代培养细胞中，1例是四倍体范围，3例是三倍体范围。Hep-2细胞系染色体众数为68～75条，出现15条可识别的标记染色体。原发性喉癌及喉癌细胞系中染色体结构异常多为末端缺失、等臂染色体和不平衡易位，而且均存在复杂的6号染色体畸变。结论6q-，i（5p），17p-，5q-可能是人类喉鳞状细胞癌特征性染色体改变；荧光原位杂交法（fluorescence in situ hybridization，FISH）可以探求常规显带方法难以确认的复杂易位和标记染色体来源，为进一步确定喉癌特征性染色体畸变提供有价值的依据。
