Skip to main page content
Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 2017 Feb 15;27(4):989-993.
doi: 10.1016/j.bmcl.2016.12.073. Epub 2016 Dec 30.

Inhibition of invasion by N-trans-feruloyloctopamine via AKT, p38MAPK and EMT related signals in hepatocellular carcinoma cells

Zhong-Tian Bai  1 , Zheng-Rong Wu  2 , Li-Li Xi  3 , Xun Li  4 , Peng Chen  2 , Fu-Qiang Wang  1 , Wen-Bo Meng  1 , Wen-Ce Zhou  1 , Xin-An Wu  3 , Xiao-Jun Yao  5 , Min Zhang  6
Affiliations

Inhibition of invasion by N-trans-feruloyloctopamine via AKT, p38MAPK and EMT related signals in hepatocellular carcinoma cells

Zhong-Tian Bai et al. Bioorg Med Chem Lett. .

Abstract

N-trans-feruloyloctopamine (FO) isolated from Garlic skin was identified as the primary antioxidant constituents, however, the effect of which on HCC invasion is still unclear. Herein, the FO was synthesized and its antitumor activities were evaluated in HCC cell lines. Cellular functional analyses have revealed that the reformed FO owns strong abilities of inhibiting cell proliferation and invasion in HCC cells. Molecular data have further showed that FO could significantly decrease the phosphorylation levels of Akt and p38 MAPK. In addition, the expression of Slug was inhibited and the level of E-cadherin increased. Molecular docking analysis indicates that the H-bond and hydrophobic interactions were critical for FO and E-cadherin binding, but FO did not seem to act directly on phosphorylated Akt and p38 MAPK. We have thus concluded that reformed FO inhibits cell invasion might be directly through EMT related signals (E-cadherin) and indirectly through PI3K/Akt, p38 MAPK signaling pathways. FO might be a promising drug in HCC treatment and prognosis.

Keywords: AKT; E-cadherin; Epithelial to mesenchymal transition (EMT); Hepatocellular carcinoma; MAPK; N-trans-feruloyloctopamine (FO).

Similar articles

See all similar articles

Cited by

See all "Cited by" articles

Publication types

MeSH terms

LinkOut - more resources