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Erschienen in: Tumor Biology 3/2016

30.09.2015 | Original Article

Repression of PES1 expression inhibits growth of gastric cancer

verfasst von: Jieping Li, Xiaodong Zhou, Xiaopeng Lan, Guobin Zeng, Xuping Jiang, Zongming Huang

Erschienen in: Tumor Biology | Ausgabe 3/2016

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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.
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Metadaten
Titel
Repression of PES1 expression inhibits growth of gastric cancer
verfasst von
Jieping Li
Xiaodong Zhou
Xiaopeng Lan
Guobin Zeng
Xuping Jiang
Zongming Huang
Publikationsdatum
30.09.2015
Verlag
Springer Netherlands
Erschienen in
Tumor Biology / Ausgabe 3/2016
Print ISSN: 1010-4283
Elektronische ISSN: 1423-0380
DOI
https://doi.org/10.1007/s13277-015-4069-8

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