4.7 Article

VLDL and LDL, but not HDL, promote breast cancer cell proliferation, metastasis and angiogenesis

期刊

CANCER LETTERS
卷 388, 期 -, 页码 130-138

出版社

ELSEVIER IRELAND LTD
DOI: 10.1016/j.canlet.2016.11.033

关键词

Breast cancer; Lipoprotein; Metastasis; VLDL; LDL

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资金

  1. Kaohsiung Medical University Hospital [KMUH102-2T07, KMUH103-3R28, KMUH104-4R29]
  2. Kaohsiung Medical University [KMU-DT103010, KMU-DT105008, KMU-DT106004, KMU-TP103D18, KMU-TP104D17]
  3. Ministry of Health and Welfare of Taiwan [MOHW104-TDU-B-212-124-003, MOHW105-TDU-B-212-134007]

向作者/读者索取更多资源

Abnormal lipoprotein profiles are associated with breast cancer progression. However, the mechanisms linking abnormal lipoprotein levels to breast cancer, progression, especially metastasis, remain unclear. Herein, we found that L1 and L5 subfractions of LDL and VLDL, but not HDL, enhanced breast cancer cell viability. L1, L5, and VLDL also increased the in vitro tumorigenesis of breast cancer cells in anchorage independent soft agar assay. In addition, L1 L5, and VLDL, but not HDL, increased the levels of mesenchymal markers Slug, Vimentin, and (beta-Catenin, and promoted breast cancer cell migration and invasion. L1, L5, and VLDL increased Akt Ser473 phosphorylation and promoted cell migration, which were reversed by the PI3K/Akt inhibitor wortmannin. Further in vitro angiogenesis assay and cytokine array analysis demonstrated that L1, L5, and VLDL enhanced secretion of angiogenic factors in breast cancer cells and promoted angiogenic activity. However, only VLDL reduced anchorage-dependent cell death and promoted lung metastasis in nude mice. In summary, our data suggest that L1, L5, and especially VLDL promote breast cancer progression and metastasis through Akt-induced EMT and angiogenesis, and provide a novel mechanism of how dyslipoproteinemia promotes breast cancer progression. (C) 2016 Elsevier Ireland Ltd. All rights reserved.

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