ArticlePharmacological reports : PR2022
Palbociclib regulates intracellular lipids in mammary tumor cells by secreting lipoprotein lipase.
Article in Pharmacological reports : PR, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed, 3 citations in OpenAlex.
- Will AMPK be a potential therapeutic target for hepatocellular carcinoma?American journal of cancer research · 2024Review
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Authors and funding
3 authors at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
backgroundLipoprotein metabolism is essential for the growth and proliferation of cancer cells, and is involved in the supply of energy and cellular components. Lipoprotein lipase (LPL) is a very important enzyme in lipoprotein metabolism; however, the details underlying the mechanism of LPL secretion are unclear. Palbociclib is an antitumor drug that inhibits cell cycle progression and suppresses the growth of cancer cells. The effects of palbociclib on energy metabolism, particularly on lipid metabolism, have not been fully elucidated.
methodsWe examined the regulation of LPL secretion, which is primarily involved in lipoprotein metabolism. FM3A mouse mammary tumor cells, which are hormone receptor-positive breast cancer cells, were treated with palbociclib, and the activity and protein levels of secreted LPL were measured. Moreover, the changes in intracellular lipid content were measured by fluorescence staining using Nile Red.
resultsFM3A cells were treated with palbociclib, the activity and protein content of secreted LPL were increased. The stimulatory secretion of LPL by palbociclib was suppressed by an intracellular Ca
conclusionsOur data suggest that palbociclib causes intracellular lipid accumulation in breast cancer cells by stimulating Ca
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