ArticleOncogene2001
Modulation of phospholipase D by hexadecylphosphorylcholine: a putative novel mechanism for its antitumoral activity.
Article in Oncogene, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
8 citing papers in PubMed, 41 citations in OpenAlex.
- Mast Cell Activation and Microtubule Organization Are Modulated by Miltefosine Through Protein Kinase C Inhibition.Frontiers in immunology · 2018Article
- Choline metabolism in malignant transformation.Nature reviews. Cancer · 2011Review
- Erucylphosphocholine induces growth inhibition, cell cycle arrest, and apoptosis in human choriocarcinoma cells.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2011Article
- The alkylphospholipid, perifosine, radiosensitizes prostate cancer cells both in vitro and in vivo.Radiation oncology (London, England) · 2011Article
- Alterations in the homeostasis of phospholipids and cholesterol by antitumor alkylphospholipids.Lipids in health and disease · 2010Article
- Miltefosine affects lipid metabolism in Leishmania donovani promastigotes.Antimicrobial agents and chemotherapy · 2007Article
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Corrections and comments
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hexadecylphosphorylcholine (HePC, D-18506, INN: Mitelfosine) belongs to the family of alkylphosphocholines with anticancer activity. Previous reports have related its antitumoral activity to their ability to interfere with phospholipid metabolism. However a clear mechanism of action has not been established yet. We have investigated the effect of HePC on two enzymes recently reported to play a role in cell growth proliferation, phospholipase D (PLD) and choline kinase (ChoK). Our results demonstrate that treatment with HePC induces a rapid stimulation of PLD, that may be achieved by PKC dependent or independent mechanisms, depending on the cell line investigated. Both PLD1 and PLD2 isoenzymes are sensitive to HePC activation. By contrast, no effect was observed by HePC on ChoK, a new target for anticancer drug development. Furthermore, in all cell lines tested, a chronic exposure of the cells to HePC abrogates PLD activation by either phorbol esters or HePC itself with no effect on total cellular PLD levels. This is reflected in a strong inhibition of PLD activity. We suggest that the inhibitory effects on PLD by HePC may be related to its antitumoral action.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.