S100A8 mediates the activation of P65/HLA-B/S100A8/BCL-2/Caspase-9 (-3) pathway in laryngeal carcinogenesis

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	S100A8 mediates the activation of P65/HLA-B/S100A8/BCL-2/Caspase-9 (-3) pathway in laryngeal carcinogenesis
其他题名	S100A8 mediates the activation of P65/HLA-B/S100A8/BCL-2/Caspase-9 ( -3 ) pathway in laryngeal carcinogenesis
	Huang DaiFa; Fu WeiNeng; Guo Yan; Xu ZhenMing; Sun XingHe; Sun KaiLai
	2008
发表期刊	CHINESE SCIENCE BULLETIN
ISSN	1001-6538
卷号	53 期号:13 页码:2017-2024
摘要	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 immunohistochemistry staining were applied to evaluate the expression levels of IKK alpha, 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 IKK alpha, 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.
其他摘要	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 immunohistochemistry 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.
关键词	CALCIUM-BINDING PROTEINS KAPPA-B GENE-EXPRESSION MRP14 S100A9 CANCER CARCINOMA INFLAMMATION DIFFERENTIATION ADENOCARCINOMA CALGRANULINS laryngeal squamous cell carcinoma (LSCC) S100A8 NF-Kappa B apoptosis HLA-B
收录类别	CSCD
语种	英语
CSCD记录号	CSCD:3435522
引用统计
文献类型	期刊论文
条目标识符	http://ir.imr.ac.cn/handle/321006/142243
专题	中国科学院金属研究所
作者单位	中国科学院金属研究所
推荐引用方式 GB/T 7714	Huang DaiFa,Fu WeiNeng,Guo Yan,et al. S100A8 mediates the activation of P65/HLA-B/S100A8/BCL-2/Caspase-9 (-3) pathway in laryngeal carcinogenesis[J]. CHINESE SCIENCE BULLETIN,2008,53(13):2017-2024.
APA	Huang DaiFa,Fu WeiNeng,Guo Yan,Xu ZhenMing,Sun XingHe,&Sun KaiLai.(2008).S100A8 mediates the activation of P65/HLA-B/S100A8/BCL-2/Caspase-9 (-3) pathway in laryngeal carcinogenesis.CHINESE SCIENCE BULLETIN,53(13),2017-2024.
MLA	Huang DaiFa,et al."S100A8 mediates the activation of P65/HLA-B/S100A8/BCL-2/Caspase-9 (-3) pathway in laryngeal carcinogenesis".CHINESE SCIENCE BULLETIN 53.13(2008):2017-2024.