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Authors Sun M, Chen Z, Tan S, Liu C, Zhao W
Received 28 November 2017
Accepted for publication 31 January 2018
Published 5 April 2018 Volume 2018:11 Pages 1961—1971
DOI https://doi.org/10.2147/OTT.S158275
Checked for plagiarism Yes
Review by Single-blind
Peer reviewers approved by Dr Colin Mak
Peer reviewer comments 2
Editor who approved publication: Dr Carlos Vigil Gonzales
Background: FSIP1 plays a vital role in tumorigenesis and cancer progression. In
bladder cancer, FSIP1 overexpression was associated with poor prognosis of
bladder urothelial carcinoma. In this study, we investigated whether FSIP1 is
essential in the progression of bladder cancer and the mechanism by which it
mediates this effect.
Methods: FSIP1 expression was knocked down in bladder cancer cells using
lentiviral-mediated short hairpin RNA (shRNA). FSIP1 expression was detected
using Western blotting, immunohistochemistry (IHC), and quantitative reverse transcriptase-polymerase
chain reaction (qRT-PCR). The effects of FSIP1 knockdown on tumor cells were
assessed using colony formation,
3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT), and flow
cytometry (FCM) apoptosis assays in vitro and BALB/c nude mouse xenograft model
in vivo.
Results: The findings suggested that FSIP1 protein was highly expressed in
bladder cancer cell lines. Knockdown of FSIP1 resulted in reduced tumor cell
viability, cell cycle arrest at G0/G1 phase and
apoptosis of bladder cancer cell lines (P <0.05).
Moreover, knockdown of FSIP1 expression suppressed the tumor formation and
growth of bladder cancer xenografts (P <0.05). At the
gene level, knockdown of FSIP1 expression downregulated the activity of the
PI3K/AKT signaling pathway.
Conclusion: This study demonstrated that knockdown of FSIP1 suppressed bladder
cancer cell malignant behaviors in vitro and in vivo through the inhibition of
the PI3K/AKT signaling pathway, suggesting that targeting FSIP1 could be
further evaluated as a potential therapeutic strategy in bladder cancer.
Keywords: bladder urothelial carcinoma, FSIP1, proliferation, apoptosis,
tumorigenicity