ApoA-I mimetic administration, but not increased apoA-I-containing HDL, inhibits tumour growth in a mouse model of inherited breast cancer

Hiperlipoproteïnes Cell Survival Lipoproteins Oncology and Carcinogenesis 610 Antineoplastic Agents Breast Neoplasms Mice, Transgenic Cardiovascular Transgenic Article LDL Càncer de mama Mice 03 medical and health sciences Breast cancer 616 Breast Cancer 2.1 Biological and endogenous factors Transgenic mice Animals Humans Aetiology Cancer Cell Proliferation High density lipoproteins 0303 health sciences Biomedical and Clinical Sciences Apolipoprotein A-I Molecular Mimicry Atherosclerosis Xenograft Model Antitumor Assays 3. Good health Lipoproteins, LDL MCF-7 Cells Female Pèptids Peptides Ratolins transgènics
DOI: 10.1038/srep36387 Publication Date: 2016-11-03T10:14:22Z
ABSTRACT
Abstract Low levels of high-density lipoprotein cholesterol (HDLc) have been associated with breast cancer risk, but several epidemiologic studies reported contradictory results regard to the relationship between apolipoprotein (apo) A-I and cancer. We aimed determine effects human apoA-I overexpression administration specific mimetic peptide (D-4F) on tumour progression by using mammary virus-polyoma middle T-antigen transgenic (PyMT) mice as a model inherited Expression in did not affect onset growth PyMT mice, despite an increase HDLc level. In contrast, D-4F treatment significantly increased latency inhibited development tumours. The were independent 27-hydroxycholesterol. However, reduced plasma oxidized low-density (oxLDL) prevented oxLDL-mediated proliferative response adenocarcinoma MCF-7 cells. conclusion, our study shows that D-4F, apoA-I-containing HDL, hinders association higher protection against LDL oxidative modification.
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