title: Repression of PES1 expression inhibits growth of gastric cancer.
abstract: Gastric cancer is one of the leading causes of cancer death worldwide. However, precise molecular mechanisms underlining its development are far from clear. We recently reported that PES1 promoted development of breast cancer and ovarian cancer as an oncogene. In this study, we reported that ablation of endogenous PES1 resulted in significant suppression of cell proliferation and growth and led to cell cycle arrest in G2 or G1 phase, respectively, in two gastric cancer cell lines (AGS and N87) in vitro. Meanwhile, silencing of PES1 obviously decreased expressions of cyclin D1, HIF-1α, and vascular endothelial growth factor (VEGF) expressions and increased p21WAF1 expression. Re-expression of PES1 in these two kinds of PES1 knockdown cells rescued these effects. In vivo, repression of endogenous PES1 expression suppressed gastric tumor growth in nude mice. In addition, 40.7 % (24/59) of gastric cancer tissues showed PES1 expression via immunohistochemical (IHC) staining. However, there were not any positive PES1 stainings in matched adjacent tissues. Our results demonstrated that repression of PES1 changed expressions of some cell proliferation- and angiogenesis-related genes and inhibited gastric cancer growth, and PES1 expression increased in gastric cancer tissues. These results suggest that PES1 may play an important role in development of gastric cancer. PES1 may be a potential target for gastric cancer therapy.
authors.affiliation: Department of Clinic Medical Laboratory, General Hospital of Fujian Corps of CAPF, Fuzhou, 350003, China. liejieping@hotmail.com.
authors.forename: Jieping
authors.initials: J
authors.lastname: Li
authors.affiliation: Department of Gastroenterology, The First Affiliated Hospital of Nanchang University, Nanchang, 330006, China.
authors.forename: Xiaodong
authors.initials: X
authors.lastname: Zhou
authors.affiliation: Institute of Clinic Laboratory Medicine, Fuzhou General Hospital of Nanjing Military Command, PLA, Fuzhou, 350003, China. lanxp@sina.com.
authors.forename: Xiaopeng
authors.initials: X
authors.lastname: Lan
authors.affiliation: Department of Clinic Medical Laboratory, General Hospital of Fujian Corps of CAPF, Fuzhou, 350003, China.
authors.forename: Guobin
authors.initials: G
authors.lastname: Zeng
authors.affiliation: Department of Clinic Medical Laboratory, General Hospital of Fujian Corps of CAPF, Fuzhou, 350003, China.
authors.forename: Xuping
authors.initials: X
authors.lastname: Jiang
authors.affiliation: Department of Pathology, General Hospital of Fujian Corps of CAPF, Fuzhou, 350003, China.
authors.forename: Zongming
authors.initials: Z
authors.lastname: Huang
mesh_terms: D000818:Animals; D045744:Cell Line, Tumor; D049109:Cell Proliferation; D006801:Humans; D051379:Mice; D008807:Mice, Inbred BALB C; D011506:Proteins / Q000032:analysis / Q000502:physiology*; D016601:RNA-Binding Proteins; D013274:Stomach Neoplasms / Q000098:blood supply / Q000209:etiology / Q000473:pathology*
chemical_list: C484463:PES1 protein, human; D011506:Proteins; D016601:RNA-Binding Proteins
keywords: Gastric cancer; PES1