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2016 ; 7
(40
): 65374-65388
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ST6Gal-I overexpression facilitates prostate cancer progression via the
PI3K/Akt/GSK-3?/?-catenin signaling pathway
#MMPMID27588482
Wei A
; Fan B
; Zhao Y
; Zhang H
; Wang L
; Yu X
; Yuan Q
; Yang D
; Wang S
Oncotarget
2016[Oct]; 7
(40
): 65374-65388
PMID27588482
show ga
ST6Gal-I sialyltransferase adds ?2,6-linked sialic acids to the terminal ends of
glycan chains of glycoproteins and glycolipids. ST6Gal-I is reportedly
upregulated in many cancers, including hepatocellular carcinoma, ovarian cancer
and breast cancer. However, the expression and function of ST6Gal-I in prostate
cancer (PCa) and the mechanism underlying this function remain largely unknown.
In this study, we observed that ST6Gal-I expression was upregulated in human PCa
tissues compared to non-malignant prostate tissues. High ST6Gal-I expression was
positively correlated with Gleason scores, seminal vesicle involvement and poor
survival in patients with PCa. ST6Gal-I knockdown in aggressive prostate cancer
PC-3 and DU145 cells significantly inhibited the proliferation, growth, migration
and invasion capabilities of these cells. ST6Gal-I knockdown decreased the levels
of several PI3K/Akt/GSK-3?/ ?-catenin pathway components, such as p-PI3K,
(Ser473)p-Akt, (Ser9)p-GSK-3? and ?-catenin. Furthermore, targeting this pathway
with a PI3K inhibitor or Akt RNA interference decreased p-Akt, p-GSK-3? and
?-catenin expression, resulting in decreased PC-3 and DU145 proliferation,
migration and invasion. Taken together, these results indicate that ST6Gal-I
plays a critical role in cell proliferation and invasion via the
PI3K/Akt/GSK-3?/?-catenin signaling pathway during PCa progression and that it
might be a promising target for PCa prognosis determination and therapy.
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