When p53 is activated, it can mend DNA damage and eliminate cancer cells by binding to DNA. How p53 maintains its basal level and becomes activated remain elusive, but identifying transcription factor PHF20 and understanding its interaction with p53 and its induction of p53 protein stability and transcription has provided a clue.
To determine whether the absence of PHF20 might regulate stress-induced p53 expression, the researchers “knocked down” PHF20. In doing so, they demonstrated that in the absence of PHF20, p53 was reduced. These findings established the role of PHF20 as a key regulator of p53 and additional link between Akt and p53.
According to Cheng, the identification of PHF20 as a regulator of p53 is significant because PHF20 “participates in simultaneous multiple interactions with other proteins and DNA” and serves to stabilize and induce p53.“Regulation of p53 is critical to allow both normal cell growth and tumor suppression,” explained Cheng. “However, further investigation is required to understand PHF20 tumor suppressor function and its possible involvement in human malignancy.”
Kim Polacek | EurekAlert!
Show me your leaves - Health check for urban trees
12.12.2017 | Gesellschaft für Ökologie e.V.
Liver Cancer: Lipid Synthesis Promotes Tumor Formation
12.12.2017 | Universität Basel
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