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2016 ; 7
(43
): 70447-70461
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A vicious cycle between acid sensing and survival signaling in myeloma cells:
acid-induced epigenetic alteration
#MMPMID27626482
Amachi R
; Hiasa M
; Teramachi J
; Harada T
; Oda A
; Nakamura S
; Hanson D
; Watanabe K
; Fujii S
; Miki H
; Kagawa K
; Iwasa M
; Endo I
; Kondo T
; Yoshida S
; Aihara KI
; Kurahashi K
; Kuroda Y
; Horikawa H
; Tanaka E
; Matsumoto T
; Abe M
Oncotarget
2016[Oct]; 7
(43
): 70447-70461
PMID27626482
show ga
Myeloma (MM) cells and osteoclasts are mutually interacted to enhance MM growth
while creating acidic bone lesions. Here, we explored acid sensing of MM cells
and its role in MM cell response to acidic conditions. Acidic conditions
activated the PI3K-Akt signaling in MM cells while upregulating the pH sensor
transient receptor potential cation channel subfamily V member 1 (TRPV1) in a
manner inhibitable by PI3K inhibition. The acid-activated PI3K-Akt signaling
facilitated the nuclear localization of the transcription factor Sp1 to trigger
the expression of its target genes, including TRPV1 and HDAC1. Consistently,
histone deacetylation was enhanced in MM cells in acidic conditions, while
repressing a wide variety of genes, including DR4. Indeed, acidic conditions
deacetylated histone H3K9 in a DR4 gene promoter and curtailed DR4 expression in
MM cells. However, inhibition of HDAC as well as either Sp1 or PI3K was able to
restore DR4 expression in MM cells suppressed in acidic conditions. These results
collectively demonstrate that acid activates the TRPV1-PI3K-Akt-Sp1 signaling in
MM cells while inducing HDAC-mediated gene repression, and suggest that a
positive feedback loop between acid sensing and the PI3K-Akt signaling is formed
in MM cells, leading to MM cell response to acidic bone lesions.
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