Vitamin K-dependent procoagulant in cancer cells: A potential target for the antimetastatic effect of warfarin?

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Abstract

Anticoagulants of the coumarin type have long been reported to inhibit metastasis growth in experimental animals; however, the mechanisms of such effects has not been clarified. Systemic anticoagulation per se does not appear to account completely for such metastasis growth depression. More recent information gathered on a cell procoagulant activity, which is vitamin K-dependent, could probably supply a fresh insight into this problem. Indeed, vitamin K deficiency induced either dietarily or pharmacologically by warfarin, does inhibit the activity of a cysteine protease with direct factor-X-activating properties. This protease is only present in warfarin-sensitive tumors. The correlation of this activity with cancer cell invasiveness is supported by experimental data in metastatic variants and, lately, also by the observation of markedly higher cancer procoagulant activity in extracts from metastases than from primary human melanomas.

Original languageEnglish
Pages (from-to)288-294
Number of pages7
JournalPathophysiology of Haemostasis and Thrombosis
Volume16
Issue number3-4
DOIs
Publication statusPublished - 1986

Fingerprint

cancer procoagulant
Vitamin K
Warfarin
Neoplasm Metastasis
Vitamin K Deficiency
Factor X
Cysteine Proteases
Growth
Anticoagulants
Melanoma
Neoplasms
Peptide Hydrolases
Observation

Keywords

  • Cancer procoagulant
  • Metastases
  • Vitamin K
  • Warfarin

ASJC Scopus subject areas

  • Hematology
  • Physiology (medical)

Cite this

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title = "Vitamin K-dependent procoagulant in cancer cells: A potential target for the antimetastatic effect of warfarin?",
abstract = "Anticoagulants of the coumarin type have long been reported to inhibit metastasis growth in experimental animals; however, the mechanisms of such effects has not been clarified. Systemic anticoagulation per se does not appear to account completely for such metastasis growth depression. More recent information gathered on a cell procoagulant activity, which is vitamin K-dependent, could probably supply a fresh insight into this problem. Indeed, vitamin K deficiency induced either dietarily or pharmacologically by warfarin, does inhibit the activity of a cysteine protease with direct factor-X-activating properties. This protease is only present in warfarin-sensitive tumors. The correlation of this activity with cancer cell invasiveness is supported by experimental data in metastatic variants and, lately, also by the observation of markedly higher cancer procoagulant activity in extracts from metastases than from primary human melanomas.",
keywords = "Cancer procoagulant, Metastases, Vitamin K, Warfarin",
author = "Donati, {Maria Benedetta} and Roncaglioni, {Maria Carla} and Anna Falanga and Bruno Casali and Nicola Semeraro",
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journal = "Pathophysiology of Haemostasis and Thrombosis",
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TY - JOUR

T1 - Vitamin K-dependent procoagulant in cancer cells

T2 - A potential target for the antimetastatic effect of warfarin?

AU - Donati, Maria Benedetta

AU - Roncaglioni, Maria Carla

AU - Falanga, Anna

AU - Casali, Bruno

AU - Semeraro, Nicola

PY - 1986

Y1 - 1986

N2 - Anticoagulants of the coumarin type have long been reported to inhibit metastasis growth in experimental animals; however, the mechanisms of such effects has not been clarified. Systemic anticoagulation per se does not appear to account completely for such metastasis growth depression. More recent information gathered on a cell procoagulant activity, which is vitamin K-dependent, could probably supply a fresh insight into this problem. Indeed, vitamin K deficiency induced either dietarily or pharmacologically by warfarin, does inhibit the activity of a cysteine protease with direct factor-X-activating properties. This protease is only present in warfarin-sensitive tumors. The correlation of this activity with cancer cell invasiveness is supported by experimental data in metastatic variants and, lately, also by the observation of markedly higher cancer procoagulant activity in extracts from metastases than from primary human melanomas.

AB - Anticoagulants of the coumarin type have long been reported to inhibit metastasis growth in experimental animals; however, the mechanisms of such effects has not been clarified. Systemic anticoagulation per se does not appear to account completely for such metastasis growth depression. More recent information gathered on a cell procoagulant activity, which is vitamin K-dependent, could probably supply a fresh insight into this problem. Indeed, vitamin K deficiency induced either dietarily or pharmacologically by warfarin, does inhibit the activity of a cysteine protease with direct factor-X-activating properties. This protease is only present in warfarin-sensitive tumors. The correlation of this activity with cancer cell invasiveness is supported by experimental data in metastatic variants and, lately, also by the observation of markedly higher cancer procoagulant activity in extracts from metastases than from primary human melanomas.

KW - Cancer procoagulant

KW - Metastases

KW - Vitamin K

KW - Warfarin

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