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Use of a Monocyte Monolayer Assay to Evaluate Fcγ Receptor-mediated Phagocytosis
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Morphine contributed to the deterioration of cancer via miR-543/MARCKS/FcγR-mediated phagocytosis pathway

Jianghui Luo1, Yiding Chen1, Yiquan Xu1

  • 1Department of Anesthesiology, Sichuan Cancer Hospital & Institute, Sichuan Cancer Center, School of Medicine, University of Electronic Science and Technology of China, Chengdu, China.

The Journal of Pharmacy and Pharmacology
|August 3, 2019
PubMed
Abstract

Insights

Morphine influences cancer progression by altering microRNA-543 (miR-543) and MARCKS expression. This modulation affects cell viability, apoptosis, and FcγR-mediated phagocytosis, impacting tumor growth.

Area of Science:

  • Oncology
  • Molecular Biology
  • Pharmacology

Background:

  • Morphine is known to negatively impact cancer patients.
  • Understanding the precise mechanisms of morphine's effect on cancer is crucial.

Purpose of the Study:

  • To elucidate the molecular mechanisms by which morphine influences cancer development.
  • To investigate the roles of MARCKS and miR-543 in morphine-induced cancer progression.

Main Methods:

  • Microarray and Gene Set Enrichment Analysis (GSEA) were employed to identify differentially expressed genes and pathways.
  • In vitro and in vivo assays were conducted to validate findings.

Main Results:

  • Morphine treatment led to decreased MARCKS and increased miR-543 expression.
  • MiR-543 promoted cell viability and tumor growth while inhibiting apoptosis.
  • MARCKS counteracted miR-543's effects and activated FcγR-mediated phagocytosis.

Conclusions:

  • Morphine at 10⁻⁶ mol/l upregulates miR-543, downregulates MARCKS, and inhibits FcγR-mediated phagocytosis.
  • This pathway contributes to cancer progression in vitro and in vivo.
  • Targeting this pathway may offer therapeutic strategies for cancer patients using morphine.
Keywords:
MARCKSFcγR-mediated phagocytosis pathwaycancermiR-543morphine

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