<p>Breast cancer remains a significant clinical challenge, with treatment failure and patient mortality primarily attributable to tumor metastasis. Daucosterol linoleate (DL) was previously isolated from sweet potato (<i>Ipomoea batatas</i>). Using HPLC analysis of ten commercial dried sweet potato products from different regions of China, DL was detected in all samples, with concentrations ranging from 1.24&#xa0;mg to 6.05&#xa0;mg per 100&#xa0;g, confirming its widespread presence in commercially processed sweet potato products. Pharmacokinetic analysis showed that DL exhibited a peak plasma concentration (C<sub>max</sub>) of 1452.28&#xa0;ng/mL, an elimination half-life (t<sub>1/2</sub>) of 11.14&#xa0;h, and a mean residence time (MRT) of 9.62&#xa0;h, supporting its potential for oral administration. DL significantly suppressed proliferation and migration of MCF-7, 4T1, and MDA-MB-231 cells in vitro and reduced lung metastasis in vivo. Proteomic analysis identified SCD1 as a key molecule mediating the effects of DL. Mechanistically, DL downregulated SCD1 to inhibit epithelial-mesenchymal transition (EMT), as evidenced by decreased expression of N-Cadherin, MMP2, Vimentin, and Snail, alongside increased E-Cadherin expression. Collectively, DL inhibits breast cancer metastasis by downregulating SCD1 and suppressing EMT, supporting its dual potential as a functional food ingredient and adjuvant therapeutic.</p>

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Daucosterol linoleate from sweet potato inhibits breast cancer metastasis via SCD1 downregulation and suppression of epithelial-mesenchymal transition

  • Xintong He,
  • Juan Li,
  • Jun Lu,
  • Zhaomin Chen,
  • Ya Wang,
  • Kehui He,
  • Xuegang Li,
  • Hang Ma,
  • Xiaoli Ye

摘要

Breast cancer remains a significant clinical challenge, with treatment failure and patient mortality primarily attributable to tumor metastasis. Daucosterol linoleate (DL) was previously isolated from sweet potato (Ipomoea batatas). Using HPLC analysis of ten commercial dried sweet potato products from different regions of China, DL was detected in all samples, with concentrations ranging from 1.24 mg to 6.05 mg per 100 g, confirming its widespread presence in commercially processed sweet potato products. Pharmacokinetic analysis showed that DL exhibited a peak plasma concentration (Cmax) of 1452.28 ng/mL, an elimination half-life (t1/2) of 11.14 h, and a mean residence time (MRT) of 9.62 h, supporting its potential for oral administration. DL significantly suppressed proliferation and migration of MCF-7, 4T1, and MDA-MB-231 cells in vitro and reduced lung metastasis in vivo. Proteomic analysis identified SCD1 as a key molecule mediating the effects of DL. Mechanistically, DL downregulated SCD1 to inhibit epithelial-mesenchymal transition (EMT), as evidenced by decreased expression of N-Cadherin, MMP2, Vimentin, and Snail, alongside increased E-Cadherin expression. Collectively, DL inhibits breast cancer metastasis by downregulating SCD1 and suppressing EMT, supporting its dual potential as a functional food ingredient and adjuvant therapeutic.