Emerging role of N-myc downstream-regulated gene 2 (NDRG2) in cancer

Wei Hu, Chongxi Fan, Peng Jiang, Zhiqiang Ma, Xiaolong Yan, Shouyin Di, Shuai Jiang, Tian Li, Yedong Cheng and Yang Yang _

PDF  |  HTML  |  How to cite

Oncotarget. 2016; 7:209-223. https://doi.org/10.18632/oncotarget.6228

Metrics: PDF 2696 views  |   HTML 3370 views  |   ?  


Wei Hu1,*, Chongxi Fan2,*, Peng Jiang3,*, Zhiqiang Ma2, Xiaolong Yan2, Shouyin Di2, Shuai Jiang4, Tian Li1, Yedong Cheng3 and Yang Yang1

1 Department of Biomedical Engineering, The Fourth Military Medical University, Xi’an, China

2 Department of Thoracic Surgery, Tangdu Hospital, The Fourth Military Medical University, Xi’an, China

3 Department of Orthopaedics, The 82th Hospital of PLA, Huaian, China

4 Department of Aerospace Medicine, The Fourth Military Medical University, Xi’an, China

* These authors have contributed equally to this work

Correspondence to:

Yang Yang, email:

Yedong Cheng, email:

Keywords: N-myc downstream-regulated gene 2, cancer, pathological processes, molecular pathways

Received: August 10, 2015 Accepted: October 06, 2015 Published: October 25, 2015


N-myc downstream-regulated gene 2 (NDRG2) is a tumor suppressor and cell stress-related gene. NDRG2 is associated with tumor incidence, progression, and metastasis. NDRG2 regulates tumor-associated genes and is regulated by multiple conditions, treatments, and protein/RNA entities, including hyperthermia, trichostatin A and 5-aza-2’-deoxycytidine, which are promising potential cancer therapeutics. In this review, we discuss the expression as well as the clinical and pathological significance of NDRG2 in cancer. The pathological processes and molecular pathways regulated by NDRG2 are also summarized. Moreover, mechanisms for increasing NDRG2 expression in tumors and the potential directions of future NDRG2 research are discussed. The information reviewed here should assist in experimental design and increase the potential of NDRG2 as a therapeutic target for cancer.

Creative Commons License All site content, except where otherwise noted, is licensed under a Creative Commons Attribution 3.0 License.
PII: 6228