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Authors Liu Y, Wang X, Zhang Z, Xiao B, An B, Zhang J
Received 13 August 2018
Accepted for publication 13 January 2019
Published 4 March 2019 Volume 2019:12 Pages 1815—1824
DOI https://doi.org/10.2147/OTT.S183748
Checked for plagiarism Yes
Review by Single-blind
Peer reviewers approved by Dr Colin Mak
Peer reviewer comments 2
Editor who approved publication: Dr Yao Dai
Background: Rab9 is a
small GTPase that localizes to the trans-Golgi Network (TGN) and late endosomes
and is involved in the recycling of mannose-6-phosphate receptors (MPRs).
Materials and methods: To
determine new treatment strategies for breast cancer and to elucidate the
mechanism underlying the phenomenon, we investigated the effects of Rab9 in the
human breast cancer cell lines MCF7 and MDA-MB-231.
Results: We
observed that knockdown of Rab9 inhibited the survival and proliferation of
MCF7 and MDA-MB-231 cells, whereas Rab9 overexpression facilitated cell
survival and proliferation by inducing or suppressing apoptosis. These results
were further confirmed by the Bax/Bcl-2 ratio in affected MCF7 and MDA-MB-231
cells, which demonstrated whether the mitochondrial apoptotic pathway was
triggered. Furthermore, the AKT/PI3K pathway is implicated in cell growth and
survival and Rab9 changed the expression and phosphorylation of PI3K signaling
pathway members. XBP1 is a key regulator of Rab9 and further confirmed that
Rab9 play important roles in breast cancer tumorigenesis.
Conclusion: These
data suggest that Rab9 is a good candidate for a novel therapeutic strategy for
the treatment of breast cancer.
Keywords: transcription
factor, proliferation, MCF7, MDA-MB-231