Disease relevance of C05689

• X-ray absorption spectroscopy has been used to investigate binding of selenohomocysteine to cobalamin-independent (MetE) and cobalamin-dependent (MetH) methionine synthase enzymes of Escherichia coli [1].
• Se-methylselenocysteine: a new compound for chemoprevention of breast cancer [2].
• Se-methylselenocysteine induces apoptosis through caspase activation and Bax cleavage mediated by calpain in SKOV-3 ovarian cancer cells [3].

High impact information on C05689

• The in vitro experiments showed that methylseleninic acid was more potent than Se-methylselenocysteine in inhibiting cell accumulation and inducing apoptosis in TM12 (wild-type p53) and TM2H (nonfunctional p53) mouse mammary hyperplastic epithelial cells, and these effects were not attributable to DNA damage, as determined by the comet assay [4].
• It is possible that these cell lines may have only a modest ability to generate a monomethylated selenium species from Se-methylselenocysteine via the beta-lyase enzyme [4].
• A functional analysis showed that the YagD protein catalyzes methylation of homocysteine, selenohomocysteine, and selenocysteine with S-adenosylmethionine and S-methylmethionine as methyl group donors [5].
• Potentiation of irinotecan sensitivity by Se-methylselenocysteine in an in vivo tumor model is associated with downregulation of cyclooxygenase-2, inducible nitric oxide synthase, and hypoxia-inducible factor 1alpha expression, resulting in reduced angiogenesis [6].
• Se-methylselenocysteine induces apoptosis mediated by reactive oxygen species in HL-60 cells [7].

Anatomical context of C05689

• It is shown that cultured cells from a selenium-accumulating Astragalus species synthesize Se-methyl-selenocysteine in contrast to those of a non-accumulating species and do not unspecifically incorporate selenium into proteins [8].
• Se-methylselenocysteine enhances PMA-mediated CD11c expression via phospholipase D1 activation in U937 cells [9].

Associations of C05689 with other chemical compounds

• Based on the above in vitro and in vivo findings, it is hypothesized that the Se-garlic extract, in part via the action of Se-methylselenocysteine, is able to inhibit tumorigenesis by suppressing the proliferation and reducing the survival of the early transformed cells [10].
• The present work determines both previously observed organoselenium species such as selenomethionine and Se-methylselenocysteine and for the first time detects the newly characterized S-(methylseleno)cysteine in plant shoots and roots when grown in the presence of selenate or selenite as the only selenium source [11].

Gene context of C05689

• Thus, selenocysteine is synthesized from selenohomocysteine and cystathionine beta-synthase and cystathionine gamma-lyase reactions [12].
• An enhancement in the fraction of p27/Kip 1-positive IDP cells, however, was detected as a result of Se-methylselenocysteine treatment [13].
• Se-methylselenocysteine activates caspase-3 in mouse mammary epithelial tumor cells in vitro [14].
• Se-methylselenocysteine (Se-MSC) has been shown to possess potent chemopreventive and anti-tumor properties [15].
• Osteopontin is a potential target gene in mouse mammary cancer chemoprevention by Se-methylselenocysteine [16].

Analytical, diagnostic and therapeutic context of C05689

• Previous research suggested that the beta-lyase-mediated production of a monomethylated selenium metabolite from Se-methylselenocysteine is a key step in cancer chemoprevention by this agent [4].
• Our working hypothesis is that GGMSC serves primarily as a carrier of Se-methylselenocysteine (MSC), which has been demonstrated in past research to be a potent cancer chemopreventive agent in animal carcinogenesis bioassays [17].
• BACKGROUND: Se-methylselenocysteine (MSC) is a naturally occurring organoselenium compound that inhibits mammary tumorigenesis in laboratory animals and in cell culture models [16].

References