Abstract
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.
Highlights
Cancer represents a large group of complex and multifactorial diseases that involve abnormal cell growth with the potential to invade other tissues [1]
To understand the role of N-myc downstream-regulated gene 2 (NDRG2) in cancer and provide insight into its mechanisms of action and potential applications, we have focused on the molecular basis of NDRG2 activity
NDRG2 expression inhibits the expression of epithelial-to-mesenchymal transition (EMT)-related genes, such as Snail, Slug, and Smadinteracting protein 1 (SIP1), and decreases EMT signaling in renal cell carcinoma [79]
Summary
Cancer represents a large group of complex and multifactorial diseases that involve abnormal cell growth with the potential to invade other tissues [1]. The down-regulation of NDRG2 expression is associated with higher tumor recurrence and lower survival rate. NDRG2 overexpression suppresses breast cancer cell adhesion and invasion.
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