HNRNPK inhibits gastric cancer cell proliferation through p53/p21/CCND1 pathway
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Hao Huang1,*, Yong Han2,3,4,*, Xingjiu Yang1, Mengyuan Li1, Ruimin Zhu1, Juanjuan Hu1, Xiaowei Zhang5, Rongfei Wei1, Kejuan Li1 and Ran Gao1
1Key Laboratory of Human Disease Comparative Medicine, Ministry of Health, Institute of Laboratory Animal Science, Chinese Academy of Medical Sciences, Beijing 100021, P. R. China
2Department of Pathology, Zhejiang Provincial People's Hospital, Hangzhou 310014, Zhejiang, P. R. China
3People's Hospital of Hangzhou Medical College, Hangzhou 310014, Zhejiang, P. R. China
4Key Laboratory of Tumor Molecular Diagnosis and Individualized Medicine of Zhejiang Province, Hangzhou 310014, Zhejiang, P. R. China
5Department of Gynaecology and Obstetrics, Civil Aviation General Hospital, Beijing 100123, P. R. China
*These authors contributed equally to this work
Ran Gao, email: [email protected]
Keywords: gastric cancer (GC), HNRNPK, proliferation
Received: September 05, 2017 Accepted: October 03, 2017 Published: October 17, 2017
Gastric cancer (GC) is one of the most common human cancers. The molecular mechanisms underlying GC carcinogenesis and progression are still not well understood. In this study, we showed that heterogeneous nuclear ribonucleoprotein K (HNRNPK) was an effective prognostic marker for GC patients especially in early stage. Overexpression of HNRNPK can retard tumor cell proliferation and colony formation in vitro and inhibit tumor growth in vivo through p53/p21/CCND1 axis. Bioinformatics analyses indicated that HNRNPK associated genes were enriched in cell cycle and DNA replication process. Protein-protein interaction network showed that HNRNPK was physically interacted with p53, p21 and other cancer related genes. Besides, GSEA showed that HNRNPK expression was positively correlated with GAMMA radiation response and DNA repair, while negatively correlated with angiogenesis, TGF-β and Hedgehog pathway activation. Finally, several chemicals including Glycine that may repress GC progression through upregulating HNRNPK are suggested. Our study demonstrated that HNRNPK may play as a tumor suppressor in gastric cancer and could be a potential therapeutic target for GC.
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