Solute carrier family 27 member 4 (Slc27a4) enhances cell growth, migration, and invasion in breast cancer cells

37Citations
Citations of this article
21Readers
Mendeley users who have this article in their library.

Abstract

Fatty acid metabolism is important in the regulation of breast cancer progression. Some of the proteins involved in fatty acid transport have been demonstrated to promote the proliferation, migration, and invasion in breast cancer cells. Solute carrier family 27 member 4 (SLC27A4) is a fatty acid transporter protein and is related to very long chain acyl-CoA synthetase activity. In the present study, bioinformatic analysis revealed that relatively high SLC27A4 expression was observed in all subtypes of breast tumor tissues when compared to normal breast tissues. Silencing SLC27A4 expression significantly reduced uptake of free fatty acids in two breast cancer cell lines, Hs578T and MDA-MB-231. Cell growth inhibition was observed in SLC27A4-silenced Hs578T and cell cycle was arrested at G2/M. In addition, the capacity of migration and invasion decreased in both cell lines after knockdown of SLC27A4. The epithelial–mesenchymal transition signaling pathway was inhibited because protein expression of Slug, vimentin, α-smooth muscle actin, and other regulators was lower than that in control cells. Taken together, our results confirm that high SLC27A4 is associated with tumor progression in breast cancer cells. It is worth investigating whether SLC27A4 serves a diagnostic marker and therapeutic target in further studies.

Cite

CITATION STYLE

APA

Yen, M. C., Chou, S. K., Kan, J. Y., Kuo, P. L., Hou, M. F., & Hsu, Y. L. (2018). Solute carrier family 27 member 4 (Slc27a4) enhances cell growth, migration, and invasion in breast cancer cells. International Journal of Molecular Sciences, 19(11). https://doi.org/10.3390/ijms19113434

Register to see more suggestions

Mendeley helps you to discover research relevant for your work.

Already have an account?

Save time finding and organizing research with Mendeley

Sign up for free