BMB Reports

생화학분자생물학회 (Korean Society for Biochemistry and Molecular Biology)
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Autocrine prostaglandin E2 signaling promotes promonocytic leukemia cell survival via COX-2 expression and MAPK pathway

  • Shehzad, Adeeb (School of Life Sciences, BK21 Plus KNU Creative BioResearch Group, Kyungpook National University) ;
  • Lee, Jaetae (Department of Nuclear Medicine, Kyungpook National University Hospital) ;
  • Lee, Young Sup (School of Life Sciences, BK21 Plus KNU Creative BioResearch Group, Kyungpook National University)
  • 투고 : 2014.04.15
  • 심사 : 2014.06.24
  • 발행 : 2015.02.28
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초록

The COX-2/$PGE_2$ pathway has been implicated in the occurrence and progression of cancer. The underlying mechanisms facilitating the production of COX-2 and its mediator, $PGE_2$, in cancer survival remain unknown. Herein, we investigated $PGE_2$-induced COX-2 expression and signaling in HL-60 cells following menadione treatment. Treatment with $PGE_2$ activated anti-apoptotic proteins such as Bcl-2 and Bcl-xL while reducing pro-apoptotic proteins, thereby enhancing cell survival. $PGE_2$ not only induced COX-2 expression, but also prevented casapse-3, PARP, and lamin B cleavage. Silencing and inhibition of COX-2 with siRNA transfection or treatment with indomethacin led to a pronounced reduction of the extracellular levels of $PGE_2$, and restored the menadione- induced cell death. In addition, pretreatment of cells with the MEK inhibitor PD98059 and the PKA inhibitor H89 abrogated the $PGE_2$-induced expression of COX-2, suggesting involvement of the MAPK and PKA pathways. These results demonstrate that $PGE_2$ signaling acts in an autocrine manner, and specific inhibition of $PGE_2$ will provide a novel approach for the treatment of leukemia.

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참고문헌

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