Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 2012 May;29(5):741-6.
doi: 10.3892/ijmm.2012.899. Epub 2012 Feb 1.

Effect of a hot water extract of Chlorella vulgaris on proliferation of IEC-6 cells

Affiliations

Effect of a hot water extract of Chlorella vulgaris on proliferation of IEC-6 cells

Seo-Hyeon Song et al. Int J Mol Med. 2012 May.

Abstract

Chlorella vulgaris, a unicellular microalgae, exerts various biological effects; however their effect on proliferation signaling pathways in normal cells has not been studied. We investigated the effect of hot water extracts of Chlorella vulgaris (CVE) on cell proliferation and related signaling pathways in rat intestinal epithelial cells (IEC-6). CVE increased the expression of insulin-like growth factor-I receptor (IGF-IR) and the phosphorylation of focal adhesion kinase (FAK) and Src. In addition, CVE induced activation of the mitogen-activated protein kinase (MAPK) and phosphatidylinositol 3-kinase (PI3K)/Akt pathways. We verified the increased phosphorylation of extracellular-signal-related kinase (ERK) and Akt and the increased expression of the PI3K regulatory subunit p85. CVE also influenced the canonical Wnt pathway through increased expression of the nuclear β-catenin, cyclin D1. Tyr-397 of FAK mediates interactions with Src homology 2 (SH2) domains in a number of other signaling proteins, including PI3K, PLC-γ, Shc, Grb7, Src and Nck2. Because CVE induced FAK activation, FAK may affect the Wnt pathway. Addition of a FAK inhibitor decreased the expression of nuclear β-catenin, cyclin D1 and c-myc, and increased the expression of cytosolic β-catenin. We conclude that CVE stimulated proliferation of IEC-6 cells via the MAPK, PI3K/Akt and canonical Wnt pathways, and that this affected the canonical Wnt pathway.

PubMed Disclaimer

Similar articles

Cited by

Publication types

MeSH terms

LinkOut - more resources