4.7 Article

Solute Carrier Family 27 Member 4 (SLC27A4) Enhances Cell Growth, Migration, and Invasion in Breast Cancer Cells

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出版社

MDPI
DOI: 10.3390/ijms19113434

关键词

solute carrier family 27 member 4 (SLC27A4); fatty acid transport protein 4 (FATP4); very long-chain acyl-CoA synthetases member 4 (ACSVL4); breast cancer; fatty acid transporter; proliferation; migration; invasion; lipid metabolism

资金

  1. Ministry of Science and Technology [MOST 104-2314-B-037-053-MY4, MOST 105-2314-B-037-037-MY3, MOST 106-2314-B-037-046, MOST 106-2320-B-037-029-MY3]
  2. Kaohsiung Medical University Hospital [KMUHS10701, KMUHS10712, KMUH106-6R34, KMUH106-6R77]
  3. Kaohsiung Medical University [KMU-DK108008]
  4. Center for Research Resources and Development of Kaohsiung Medical University

向作者/读者索取更多资源

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, -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.

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