New study below. Should interest those using heparin.
"The interaction with platelets is of crucial importance for tumor cells passing through hematogenous metastasis. Platelets protect cancer cells from immune surveillance and exhibit many other prometastatic effects. Notably, platelets can change the epithelial tumor phenotype, a process termed epithelial-mesenchymal transition (EMT), which confers stem cell-like properties onto tumor cells associated with an increased motility and drug resistance."
"Our data show that different tumor cell entities have different platelet binding capacities and also that a weak interaction is sufficient to change tumor cell phenotype. Additionally, unfractionated heparin (UFH) as well as low molecular weight heparin (LMWH) reduced tumor cell platelet interaction. Subsequently, attenuated platelet-derived mediator release resulted in reduced EMT marker protein and transcription factor expression by the cancer cells and decreased cell migration."
When I was diagnosed with DVTs in my left calf some years ago, I was given Low Molecular Weight Heparin [LMWH] while a therapeutic dose of Warfarin was determined. In fact, I was injecting LMWH for about 5 weeks.
I am puzzled by the study since my understanding is that LMWH action doesn't involve platelets. In about 1% of patients, LMWH can lead to an unwanted reduction in platelet count, however. [2]
-Patrick
[1] ncbi.nlm.nih.gov/pubmed/303...
Molecules. 2018 Oct 19;23(10). pii: E2690. doi: 10.3390/molecules23102690.
Unfractionated and Low Molecular Weight Heparin Reduce Platelet Induced Epithelial-Mesenchymal Transition in Pancreatic and Prostate Cancer Cells.
Ponert JM1, Gockel LM2, Henze S3, Schlesinger M4.
Author information
Abstract
The interaction with platelets is of crucial importance for tumor cells passing through hematogenous metastasis. Platelets protect cancer cells from immune surveillance and exhibit many other prometastatic effects. Notably, platelets can change the epithelial tumor phenotype, a process termed epithelial-mesenchymal transition (EMT), which confers stem cell-like properties onto tumor cells associated with an increased motility and drug resistance. The aim of the study is to investigate the impact of heparin on the platelet induced EMT program in pancreatic and prostate tumor cells. Platelet activation and interaction with cancer cells were determined by static adhesion assays. Applying ELISAs, the platelet release of EMT inducing mediators was quantified. EMT marker protein expression by tumor cells was explored by western blot and qPCR. Our data show that different tumor cell entities have different platelet binding capacities and also that a weak interaction is sufficient to change tumor cell phenotype. Additionally, unfractionated heparin (UFH) as well as low molecular weight heparin (LMWH) reduced tumor cell platelet interaction. Subsequently, attenuated platelet-derived mediator release resulted in reduced EMT marker protein and transcription factor expression by the cancer cells and decreased cell migration. These data suggest that heparin reduces platelet induced EMT program and prevents the formation of cancer cells with stem cell-like properties. This additional mechanism argues for the use of heparin in oncological applications.
KEYWORDS:
EMT; cancer stem cells; enoxaparin; epithelial-mesenchymal transition; heparin; platelet; tumor
PMID: 30347648 DOI: 10.3390/molecules23102690
