mevalonic acid/breast neoplasms

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The isomiR-140-3p-regulated mevalonic acid pathway as a potential target for prevention of triple negative breast cancer.

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Prevention of triple-negative breast cancer (TNBC) is hampered by lack of knowledge about the drivers of tumorigenesis.To identify molecular markers and their downstream networks that can potentially be targeted for TNBC prevention, we analyzed small RNA

Different points of action of retinoids and anti-estrogens in G1 phase identified in synchronized T-47D breast cancer cells.

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Both retinoids and anti-estrogens inhibit breast cancer cell proliferation with accumulation of cells in the G1 phase of the cell cycle, but the effect of retinoids is delayed compared to that of anti-estrogens. To determine whether this temporal difference is due to a simple delay in the action of

Alendronate inhibits invasion of PC-3 prostate cancer cells by affecting the mevalonate pathway.

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Breast and prostate cancer preferentially metastasize in the skeleton, inducing locally increased bone resorption by osteoclasts. Bisphosphonates (BPs), potent inhibitors of osteoclasts and bone resorption, are able to reduce metastatic bone lesions, but the metastasis-related cellular target

Dolichol-like lipids with stimulatory effect on DNA synthesis: substrates for protein dolichylation?

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Substantial evidence has suggested that a nonsterol product of mevalonic acid (MVA) is essential for the initiation of DNA synthesis in mammalian cells. Several possible isoprenoid candidates have been suggested, but the identity of this compound still remains unknown. In this study we have isolated

Synchronization of tumor and normal cells from G1 to multiple cell cycles by lovastatin.

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Synchronization of mammalian cells is essential for investigations involving cell proliferation. A simple method for obtaining synchrony in all types of cells, through several cycles and with minimal overall metabolic perturbations, has not yet been available. We describe a procedure for

Antitumor effects of the combination of cholesterol reducing drugs.

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There are a number of potential mechanisms linking cholesterol homeostasis to processes that are tightly linked with carcinogenesis. Statins, which are inhibitors of 3-hydroxy-3-methylglutaryl-coenzyme A reductase (HMG-CoAR), the rate-limiting enzyme in the mevalonic acid synthesis pathway, exert

Berberine, a natural cholesterol reducing product, exerts antitumor cytostatic/cytotoxic effects independently from the mevalonate pathway.

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The aim of this study was to investigate the role of the mevalonate pathway in the cytostatic/cytotoxic effects of berberine, a natural plant alkaloid that reduces cholesterol concentration. Berberine as well as lovastatin, an inhibitor of the mevalonate pathway, exerted dose-dependent

Pitavastatin inactivates NF-kappaB and decreases IL-6 production through Rho kinase pathway in MCF-7 cells.

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The aim of the present study was to provide new mechanistic insight into the effect of pitavastatin at low dose on NF-kappaB activated by TNF-alpha in the human breast cancer cell line (MCF-7). We found that treatment of MCF-7 with 1 microM pitavastatin inhibited the proliferation and suppressed the

Metabolic control of YAP and TAZ by the mevalonate pathway.

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The YAP and TAZ mediators of the Hippo pathway (hereafter called YAP/TAZ) promote tissue proliferation and organ growth. However, how their biological properties intersect with cellular metabolism remains unexplained. Here, we show that YAP/TAZ activity is controlled by the SREBP/mevalonate pathway.

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