2. Academic Validation
  3. FAM83D activates the MEK/ERK signaling pathway and promotes cell proliferation in hepatocellular carcinoma

FAM83D activates the MEK/ERK signaling pathway and promotes cell proliferation in hepatocellular carcinoma

  • Biochem Biophys Res Commun. 2015 Mar 6;458(2):313-20. doi: 10.1016/j.bbrc.2015.01.108.
Dong Wang 1,  Sheng Han 1,  Rui Peng 1,  Xing Wang 1,  Xin-Xiang Yang 1,  Ren-Jie Yang 1,  Chen-Yu Jiao 1,  Dong Ding 1,  Gu-Wei Ji 1,  Xiang-Cheng Li 2
Affiliations

Affiliations

  • 1 Liver Transplantation Center, First Affiliated Hospital of Nanjing Medical University, Key Laboratory of Living Donor Liver Transplantation, Ministry of Public Health, Nanjing, China.
  • 2 Liver Transplantation Center, First Affiliated Hospital of Nanjing Medical University, Key Laboratory of Living Donor Liver Transplantation, Ministry of Public Health, Nanjing, China. Electronic address: drxcli@njmu.edu.cn.
PMID: 25646692 DOI: 10.1016/j.bbrc.2015.01.108
Abstract

Publicly available microarray data suggests that the expression of FAM83D (Family with sequence similarity 83, member D) is elevated in a wide variety of tumor types, including hepatocellular carcinoma (HCC). However, its role in the pathogenesis of HCC has not been elucidated. Here, we showed that FAM83D was frequently up-regulated in HCC samples. Forced FAM83D expression in HCC cell lines significantly promoted their proliferation and colony formation while FAM83D knockdown resulted in the opposite effects. Mechanistic analyses indicated that FAM83D was able to activate the MEK/ERK signaling pathway and promote the entry into S phase of cell cycle progression. Taken together, these results demonstrate that FAM83D is a novel oncogene in HCC development and may constitute a potential therapeutic target in HCC.

Keywords

Cell cycle; FAM83D; HCC; MEK/ERK; Proliferation.

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