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Regulation of mPGES-1 composition and cell growth via the MAPK signaling pathway in jurkat cells

Yi-Qing Li1,2, Jiao-Ting Chen1,2,3, Song-Mei Yin1

  • 1Department of Hematology, Sun Yat-Sen Memorial Hospital, Sun Yat-Sen University, Guangzhou, Guangdong 510120, P.R. China.

Experimental and Therapeutic Medicine
|September 15, 2018
PubMed

Insights

Microsomal prostaglandin E synthase-1 (mPGES-1) plays a key role in T-cell acute lymphoblastic leukemia (T-ALL). Targeting mPGES-1 and mitogen-activated protein kinase (MAPK) pathways may offer new T-ALL therapies.

Area of Science:

  • Oncology
  • Molecular Biology
  • Immunology

Background:

  • Microsomal prostaglandin E synthase-1 (mPGES-1) is linked to MAPK pathways in cancers.
  • The role of mPGES-1 in T-cell acute lymphoblastic leukemia (T-ALL) is not well understood.

Purpose of the Study:

  • To investigate the role of mPGES-1 in T-ALL.
  • To identify interactions between mPGES-1 and the MAPK signaling pathway in T-ALL.

Main Methods:

  • RNA silencing to decrease mPGES-1 expression in T-ALL jurkat cells.
  • Microarray and western blot analyses to examine signaling pathway interactions.

Main Results:

  • mPGES-1 overexpression was reduced by RNA silencing in T-ALL jurkat cells.
  • Decreased mPGES-1 inhibited proliferation, induced apoptosis, and arrested the cell cycle.
  • c-Jun N-terminal kinase was involved in positive feedback loops, while P38 and ERK1/2 showed negative feedback on mPGES-1.

Conclusions:

  • Complex cross-talk exists between mPGES-1 and MAPK signaling in T-ALL.
  • Combined targeting of mPGES-1 and MAPK pathways could be a potential therapeutic strategy for T-ALL.
Keywords:
T-cell acute lymphoblastic leukemiafeedbackjurkat cellmicrosomal prostaglandin-E synthasemitogen activated protein Kinase Signaling System

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