Abstract
The recently described oncogene ZNF217 belongs to a chromosomal region that is frequently amplified in human cancers. Recent findings have revealed that alternative mechanisms such as epigenetic regulation also govern the expression of the encoded ZNF217 protein. Newly discovered molecular functions of ZNF217 indicate that it orchestrates complex intracellular circuits as a new key regulator of tumorigenesis. In this review, we focus on recent research on ZNF217-driven molecular functions in human cancers, revisiting major hallmarks of cancer and highlighting the downstream molecular targets and signaling pathways of ZNF217. We also discuss the exciting translational medicine investigating ZNF217 expression levels as a new powerful biomarker, and ZNF217 as a candidate target for future anti-cancer therapies.
Highlights
During tumor progression, normal cells evolve progressively to a neoplastic state through the successive acquisition of hallmark capabilities
ErbB3-driven activation of PI3K/Akt was implicated in resistance to paclitaxel [49] and, to date, the increased expression of the ErbB3 gene, a direct target for the zinc-finger protein 217 (ZNF217) transcription factor [19], is the only clearly defined mechanism associated with the ZNF217-driven activation of the PI3K/Akt pathway [19, 30]
The first evidence of this came from the observation that ZNF217 is an estrogen receptor alpha (ERα) target gene, as 17β-estradiol exposure led to ZNF217 mRNA deregulated expression in ER+ breast cancer cells [81]
Summary
Normal cells evolve progressively to a neoplastic state through the successive acquisition of hallmark capabilities. ZNF217 induced overexpression of both the Bcl-XL and Aurora-A proteins in paclitaxel-resistant ZNF217overexpressing breast cancer cells [28], and expression of BCL2L1 protein correlated with that of ZNF217 mRNA in colorectal tumors [48].
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