Cell apoptosis was detected by flow cytometry. Cell invasion was determined by transwell coated with matrigel. RKIP, phospho-RKIP, Raf-1, phospho-Raf-1, ERK1/2, phospho-ERK1/2, GRK2 and GAPDH was assayed by Western blot. LIN28 and MMP-14 mRNA was assayed by RT-qPCR. Results: The results showed RKIP expression is reduced in esophageal cancer tissues in comparison with normal esophageal epithelium tissues and tumor-adjacent tissues. Reduced RKIP expression is associated with lymph node or distant metastasis in esophageal cancer tissues. RKIP inhibits invasive and RO4929097 metastatic ability

of esophageal cancer cell line TE-1 by down-regulating mRNA expression of LIN28 and MMP-14. RKIP has no effect on MAPK signaling pathway in esophageal cancer cell line TE-1, but it is involved in G protein-coupled signaling pathway. Conclusion: Our findings clearly demonstrate that RKIP inhibits esophageal cancer cell invasion by down-regulating the expression of GRK-2, Silmitasertib manufacturer LIN28 and MMP-14. Key Word(s): 1. Esophageal cancer; 2. Invasion; 3. RKIP; 4. Proliferation; Presenting Author: ZHANG NANA Additional Authors: LI PENG, ZHANG SHUTIAN Corresponding Author: ZHANG NANA Affiliations:

beijing freindship hospital Objective: The aim of this study was to clear that NNK play a role on esophageal cells partially through beta-adrenoceptor. Methods: using RNA

interference technology to specially inhibit the expression of beta1 and beta2 receptor in human esophageal squamous carcinoma KYSE 410 cell line and normal esophageal cell line HET-1A. Blank group, negative group, interference group, blank + NNK, negative + NNK, interference + NNK groups were set. Transwell room was used to detect the influence of NNK on cell invasion and migration. we used MTT assay to detect cell proliferation and AV-PI double staining to measure MCE cell apoptosis. Expression of p-Erk1/2, VEGF, Cyclin-D1, Bcl-2 and Bax were measured by Western blot. Results: NNK promoted proliferation and inhibited apoptosis in both KYSE410 and HET-1A cell lines. In KYSE410 cell line, NNK enhanced migration and invasion. WB showed that NNK promoted expression of p-Erk1/2, VEGF, Cyclin-D1 and Bcl-2, without significant changes of Bax. Conclusion: NNK can promote cell proliferation, invasion, migration and inhibited apoptosis in esophageal cell partially through beta adrenergic receptor. Key Word(s): 1. ESCC; 2. beta-adrenoceptor; 3.