Research Papers:

HNRNPK inhibits gastric cancer cell proliferation through p53/p21/CCND1 pathway

Hao Huang, Yong Han, Xingjiu Yang, Mengyuan Li, Ruimin Zhu, Juanjuan Hu, Xiaowei Zhang, Rongfei Wei, Kejuan Li and Ran Gao _

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Oncotarget. 2017; 8:103364-103374. https://doi.org/10.18632/oncotarget.21873

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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

Correspondence to:

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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