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已发表论文
化疗通过半胱天冬酶-3 介导的花生四烯酸代谢途径诱导卵巢癌细胞再生
Authors Cui LZ, Zhao YW, Pan Y, Zheng X, Shao D, Jia Y, He K, Li K, Chen L
Received 31 August 2017
Accepted for publication 10 November 2017
Published 8 December 2017 Volume 2017:10 Pages 5817—5826
DOI https://doi.org/10.2147/OTT.S150456
Checked for plagiarism Yes
Review by Single-blind
Peer reviewers approved by Dr Akshita Wason
Peer reviewer comments 2
Editor who approved publication: Prof. Dr. Geoffrey Pietersz
Abstract: Recurrence is one of
the major causes of high mortality in ovarian cancer. However, the mechanism of
ovarian cancer recurrence after chemotherapy has not been fully understood. In
the present study, we investigated the effect of chemotherapy-induced tumor
microenvironment on the proliferation of SKOV3 cells. We have shown that SKOV3
cells repopulated faster in the culture medium from apoptotic SKOV3 ovarian
cancer cells after 24 h of etoposide phosphate (VP-16) treatment. We found that
during apoptosis, cleaved caspase 3 could activate cytosolic
calcium-independent phospholipase A2, which
stimulated the release of arachidonic acid (AA) and triggered the production of
prostaglandin E2 (PGE2). An increased level of phosphorylated focal
adhesion kinase (FAK) subsequently facilitated the reproliferation of SKOV3
cells, and VP-16-induced repopulation effects were partially reversed by the
FAK inhibitor PF562271. Furthermore, the plasma AA-to-PGE2 ratio and tumoral FAK expression of ovarian cancer
patients after chemotherapy were significantly lower than those before
chemotherapy. Taken together, our results indicate that chemotherapy-induced
apoptotic cancer cells can produce PGE2-enriched
microenvironment through caspase 3-mediated AA metabolic pathway, which could
lead to the abnormal activation of FAK and eventually accelerate the
repopulation of SKOV3 cells. Our study provides novel insight into a mechanism
that may be utilized to prevent ovarian cancer recurrence in response to
chemotherapy.
Keywords: ovarian cancer, repopulation, chemotherapy, apoptosis, FAK
Keywords: ovarian cancer, repopulation, chemotherapy, apoptosis, FAK
