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2016 ; 6
(ä): 36289
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Oncometabolite D-2-Hydroxyglurate Directly Induces Epithelial-Mesenchymal
Transition and is Associated with Distant Metastasis in Colorectal Cancer
#MMPMID27824159
Colvin H
; Nishida N
; Konno M
; Haraguchi N
; Takahashi H
; Nishimura J
; Hata T
; Kawamoto K
; Asai A
; Tsunekuni K
; Koseki J
; Mizushima T
; Satoh T
; Doki Y
; Mori M
; Ishii H
Sci Rep
2016[Nov]; 6
(ä): 36289
PMID27824159
show ga
Deranged metabolism is a hallmark of cancer, playing a significant role in
driving the disease process. One such example is the induction of carcinogenesis
by the oncometabolite D-2 hydroxyglutarate (D-2HG), which is produced by the
mutated enzyme isocitrate dehydrogenase (IDH) occurring in subsets of leukaemias
and brain tumours. The oncogenic property of D-2HG appears to stem from its
ability to interfere with the activities of ?-ketoglutarate-dependent
dioxygenases, including the Jumonji family histone demethylases. Here, we find in
colorectal cancer cells that even in the absence of IDH mutation, the levels of
D-2HG and its enantiomer L-2HG were elevated through glutamine anaplerosis.
D-2HG, but not L-2HG, increased the trimethylation of histone H3 lysine 4 of the
promoter region of ZEB1, a master regulator of epithelial-mesenchymal transition
(EMT), and increased the expression of the ZEB1 gene to directly induce EMT in
colorectal cancer cells. EMT promotes the ability of cancer cells to invade the
local tissue and enter into the bloodstream, leading to distant organ metastasis.
D-2HG levels were elevated in colorectal cancer specimens, particularly in those
associated with distant metastasis, supporting the observations in vitro and
implicating the contribution of D-2HG in metastasis, the major cause of death in
this disease.
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