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2015 ; 6
(12
): 9924-36
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HSPA12B: a novel facilitator of lung tumor growth
#MMPMID25909170
Ma H
; Lu T
; Zhang X
; Li C
; Xiong J
; Huang L
; Liu P
; Li Y
; Liu L
; Ding Z
Oncotarget
2015[Apr]; 6
(12
): 9924-36
PMID25909170
show ga
Lung tumor progression is regulated by proangiogenic factors. Heat shock protein
A12B (HSPA12B) is a recently identified regulator of expression of proangiogenic
factors. However, whether HSPA12B plays a role in lung tumor growth is unknown.
To address this question, transgenic mice overexpressing HSPA12B (Tg) and
wild-type littermates (WT) were implanted with Lewis lung cancer cells to induce
lung tumorigenesis. Tg mice showed significantly higher number and bigger size of
tumors than WT mice. Tg tumors exhibited increased angiogenesis and proliferation
while reduced apoptosis compared with WT tumors. Interestingly, a significantly
enhanced upregulation of Cox-2 was detected in Tg tumors than in WT tumors. Also,
Tg tumors demonstrated upregulation of VEGF and angiopoietin-1, downregulation of
AKAP12, and increased eNOS phosphorylation compared with WT tumors. Celecoxib, a
selective Cox-2 inhibitor, suppressed the HSPA12B-induced increase in lung tumor
burden. Moreover, celecoxib decreased angiogenesis and proliferation whereas
increased apoptosis in Tg tumors. Additionally, celecoxib reduced angiopoietin-1
expression and eNOS phosphorylation but increased AKAP12 levels in Tg tumors. Our
results indicate that HSPA12B stimulates lung tumor growth via a Cox-2-dependent
mechanism. The present study identified HSPA12B as a novel facilitator of lung
tumor growth and a potential therapeutic target for the treatment of lung cancer.
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