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Authors Liu Q, Tan W, Che J, Yuan D, Zhang L, Sun Y, Yue X, Xiao L, Jin Y
Received 16 July 2018
Accepted for publication 29 September 2018
Published 16 November 2018 Volume 2018:10 Pages 5825—5838
DOI https://doi.org/10.2147/CMAR.S180334
Checked for plagiarism Yes
Review by Single-blind
Peer reviewers approved by Dr Andrew Yee
Peer reviewer comments 3
Editor who approved publication: Professor Nakshatri
Background: The
dysfunction of cell apoptosis is an important event in the progression of
cancer, and the growth of cancer cells is negatively regulated by cell
apoptosis. In different types of cancers, inhibition of cellular apoptosis is
often observed in the cancerous tissue, and increased resistance to apoptosis
is a hallmark of cancer. Although previous studies have shown that
12-lipoxygenase (12-LOX)/12-hydroxyeicosatetraenoic acid (12-HETE) is activated
and upregulated in different types of cancers, the consequences of
12-LOX/12-HETE upregulation and its precise roles in the survival of ovarian
carcinoma cells are still unknown.
Methods: MTT
assays, caspase activity assays, lactate dehydrogenase (LDH) assays, and
Western blot analysis were the methods used in this study.
Results: In our
study, we found that 12-HETE, a major metabolic product of arachidonic acid
using 12-LOX catalysis, inhibited cell apoptosis in a dose-dependent manner and
that the effects of 12-HETE on cell apoptosis were mediated by the
integrin-linked kinase (ILK) pathway. Moreover, the downstream target of
12-HETE-activated ILK was nuclear factor kappa-B (NF-κB) in ovarian carcinoma.
The inhibitory effects of 12-HETE on cell apoptosis were attenuated by the
inhibition of the NF-κB pathway.
Conclusion: These
results indicate that 12-HETE participates in the inhibition of cell apoptosis
by activating the ILK/NF-κB pathway, implying an important underlying mechanism
that promotes the survival of ovarian cancer cells.
Keywords: 12-HETE,
ILK, apoptosis, NF-κB, ovarian cancer