Overexpression of 14-3-3σ Modulates Cholangiocarcinoma Cell Survival by PI3K/Akt Signaling. (23rd June 2020)

• Record Type: Journal Article
• Authors: Wu, Qiao; Fan, Hua; Lang, Ren; Li, Xianliang; Zhang, Xingmao; Lv, Shaocheng; He, Qiang
• Other Names: Yang Jialiang Guest Editor.
• Is Part Of: BioMed research international. Volume 2020(2020)
• Publication Date: 2020-06-23
• Subjects: Medicine -- Periodicals; Biology -- Periodicals; Biotechnology -- Periodicals; Life sciences -- Periodicals; 610.5
• DOI: 10.1155/2020/3740418
• Languages: English
• ISSNs: 2314-6133

Abstract

Abstract : The protein 14-3-3 σ is involved in numerous cellular processes through its ability to bind phosphorylated serine/threonine residues. It is a key regulator of the cell cycle involving in G2 arrest by p53. Deregulation of 14-3-3 σ expression has been associated with a large variety of human cancers. However, its physiological function and therapeutic significance have rarely been investigated in cholangiocarcinoma. Using immunohistochemistry (IHC), we evaluated 14-3-3 σ expression in 65 human extrahepatic cholangiocarcinomas. As a result, we found that 14-3-3 σ is expressed in the tissue of 56 patients (86.2%), and its expression is positively correlated with tumor size, lymph node metastasis, and tumor stage. We also explored the significance of 14-3-3 σ and found that 14-3-3 σ exerts cell type-dependent effects on cell proliferation through PI3K/Akt signaling in both in vitro and in vivo xenograft models. These results suggest that 14-3-3 σ assumes a constitutive role in tumorigenesis rather than acting as a cell cycle regulator in cholangiocarcinoma, which makes 14-3-3 σ a new potential target for therapeutic intervention.