Vitamin K2

Author: Gianpiero Pescarmona
Date: 10/08/2019



Vitamin K2 or menaquinone (MK) (/ˌmɛnəˈkwɪnoʊn/) is one of three types of vitamin K, the other two being vitamin K1 (phylloquinone) and K3 (menadione). K2 is both a tissue and bacterial product (derived from vitamin K1 in both cases) and is usually found in animal products or fermented foods.

The number n of isoprenyl units in their side chain differs and ranges from 4 to 13, hence Vitamin K2 consists of various forms. It is indicated as a suffix (-n), e. g. MK-7 or MK-9. The most common in the human diet is the short-chain, water-soluble menatetrenone (MK-4), which is usually produced by tissue and/or bacterial conversion of vitamin K1, and is commonly found in animal products. It is known that production of MK-4 from dietary plant vitamin K1 can be accomplished by animal tissues alone, as it proceeds in germ-free rodents.

Long-chain menaquinones (longer than MK-4) include MK-7, MK-8 and MK-9 and are more predominant in fermented foods such as natto. Longer-chain menaquinones (MK-10 to MK-13) are produced by anaerobic bacteria in the colon, but they are not well absorbed at this level and have little physiological impact.

n= 7-9


Vitamin k2 has a function as a Cofactor in many reactions
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Divergent effects of vitamins K1 and K2 on triple negative breast cancer cells. 2019

  • Abstract
    Vitamin K serves as an essential co-factor in the γ-carboxylation of glutamate to γ-carboxyglutamate (GLA), a post-translational modification mediated by gamma-glutamyl carboxylase (GGCX) and vitamin K oxidoreductases (VKORC1 or VKORC1L1). While both phylloquinone (K1) and menaquinone (K2) support the synthesis of GLA-modified proteins, studies assessing K1 and/or K2 effects in cancer cells have reported minimal effects of K1 and anti-proliferative or pro-apoptotic effects of K2. qPCR results indicated highest expression of GGCX, VKORC1, and VKORC1L1 in triple negative breast cancer (TNBC) cell lines, Hs578T, MDA-MB-231 and SUM159PT, and in advanced stage disease. To assess differential effects of vitamin K, TNBC cells were cultured in media supplemented with K1 or K2. K1 treatment increased cell growth, and enhanced stemness and GLA-modified protein expression in TNBC lysates. Alternatively, lysates from cells exposed to vehicle, K2, or the VKOR antagonist, warfarin, did not express GLA-modified proteins. Further, K2 exposure reduced stemness and elicited anti-proliferative effects. These studies show that TNBC cells express a functional vitamin K pathway and that K1 and K2 exert distinct phenotypic effects. Clarification of the mechanisms by which K1 and K2 induce these effects may lead to relevant therapeutic strategies for manipulating this pathway in TNBC patients.
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