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
AUTHORS (18)
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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