Li. Conclusion: These results showed we had successfully established a Hyper-IL-6-expressing mouse hepatocellular carcinoma cell clones which would enable us to further study to established a promising tumor model as a new hepatocellular carcinoma vaccine. Key Word(s): 1. Interleukin
6; 2. Hyper-IL-6; 3. tumorigenicity; RAD001 mouse Presenting Author: XIUJING SUN Additional Authors: JIHUIJ. QIU, SHENGTAO ZHU, BANGWEI CAO, LIN SUN, PENG LI, XIYIN WANG, SEN LI, SHUTIAN ZHANG, SHUO DONG Corresponding Author: SHUTIAN ZHANG, SHUO DONG Affiliations: Beijing Friendship Hospital Affiliated to Capital Medical University; Department of Medicine and Dan L. Duncan Cancer Center, Baylor College of Medicine, Houston, USA; Department of Gastroenterology, Saracatinib cost Beijing Friendship Hospital Affiliated to Capital Medical University, Beijing, China; Department of Oncology, Beijing Friendship Hospital Affiliated to Capital Medical University, Beijing, China Objective: Overexpression or mutation of some histone demethylases has been implicated in the course of esophageal squamous cell carcinoma initiation and progression. The aim of this study is to investigate the role of a new histone demethylase, PHF8 in
the caicinogenesis of ESCC. Methods: Three ESCC cell lines (TE-1, TE-2 and TE-8) were analysized in this study and each cell line was divided into three groups: PHF8-shRNA experimental group, Nonsilencing-shRNA negative group and control group. Via lentivirus mediated shRNA method, we knockdown the 上海皓元医药股份有限公司 expression of PHF8 of the studied cell lines. And stable cell lines were constructed using puromycin selection assay. Real-time PCR and Western Blot were used to confirm the silencing of PHF8. Research on the regulatory role of PHF8 on proliferation, colony formation ability, migration and invasion ability, and apoptosis of ESCC cells was carried out by cell viability assay (MTS), plate and soft agar colony formation assay,
in vitro migration and invasion assay, and flow cytometry (FCM). The effect of PHF8 on tumorigenicity of ESCC cells in vivo was performed by xenograft studies of nude mice. Results: Lentivirus mediated shRNA effectively reduced the expression of PHF8 mRNA and protein in ESCC cell lines. Knockdown of PHF8 suppressed the proliferation and colony formation ability, induced the apoptosis, and inhibited the migration and invasion activity of ESCC cells. And it also effectively inhibited the growth of tumor of human esophageal squamous cell carcinoma-bearing nude mouse. Conclusion: PHF8 is involved in the carcinogenesis of esophageal squamous cell carcinoma. Key Word(s): 1. esophageal cancer; 2. epigenetics; 3. histone demethylase; 4. PHD finger protein 8; Presenting Author: WENJI YAN Additional Authors: MINGZHOU GUO, YUNSHENG YANG, KONGMING WU, JAMESG. HERMAN, MALCOLMV.