ArticleNaunyn-Schmiedeberg's archives of pharmacology1996
Investigations on the mechanism of action of the antiproliferant and ion channel antagonist flufenamic acid.
Article in Naunyn-Schmiedeberg's archives of pharmacology, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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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
2 citing papers in PubMed, 10 citations in OpenAlex.
- Multiple action sites of flufenamate on ion transport across the rat distal colon.British journal of pharmacology · 2000Article
- Sequential activation of different Ca2+ entry pathways upon cholinergic stimulation in mouse pancreatic acinar cells.The Journal of physiology · 1999Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The compound flufenamic acid has been previously described as an inhibitor of chloride- and non-selective cation channels. Moreover, this compound showed antiproliferative effects in the mouse fibroblast cell line LM(TK-). In this study, we investigated the effects of this compound on cell proliferation and membrane currents induced by mitogens (such as fetal calf serum, FCS) or platelet-derived growth factor (PDGF) in LM(TK-) cells. After a brief application of FCS or PDGF (5-15 s), the electrical response of the cells was biphasic: First, a transient potassium conductance was activated, which appeared 8.3 +/- 0.7 s after the onset of stimulation and lasted for 30.1 +/- 2.9 s. The corresponding single channel currents in cell-attached patches had an amplitude of 3-4 pA (at a holding potential of +60 mV). The second effect of serum or PDGF was the occurrence of a cation conductance for monovalent ions (sodium, potassium and cesium) and calcium. In contrast to the potassium current, this conductance activated later (11.8 +/- 1.6 s after onset of fetal calf serum stimulation) and remained activated for minutes. Flufenamic acid inhibited the proliferation of LM(TK-) cells reversibly and in a concentration-dependent manner. This effect can be correlated with the inhibitory effects of flufenamic acid on mitogen-induced membrane currents: The compound inhibited the non-selective cation current with an IC50 of 38 microM, whereas 135 microM were necessary for halfmaximal inhibition of the potassium current; this is very close to the concentration for halfmaximal inhibition of cell proliferation (120 microM). Hence, on the grounds of this comparison the blockade of the non-selective cation current appears to be of only minor importance for the blockade of cell proliferation.
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