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Mechanism of Kemeng Fang's Inhibition of Podocyte Apoptosis in Rats with Membranous Nephropathy through the PI3K/AKT Signaling Pathway
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Synergistic effects of inhibiting the MNK-eIF4E and PI3K/AKT/ mTOR pathways on cell migration in MDA-MB-231 cells

Ella Lineham1, Graham J Tizzard2, Simon J Coles2

  • 1Department of Biochemistry, School of Life Sciences, University of Sussex, Falmer, Brighton, UK.

Oncotarget
|March 28, 2018
PubMed

Insights

Simultaneous inhibition of pathways controlling eukaryotic initiation factor 4E (eIF4E) slows breast cancer cell migration. Novel hybrid agents targeting these pathways were less effective, suggesting complex regulation of cell migration.

Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • Eukaryotic initiation factor 4E (eIF4E) regulates the translation of proteins crucial for aggressive tumor cell migration.
  • The eIF4F complex, including eIF4E, is a key determinant of mRNA translation.
  • Mitogen-activated protein kinase interacting kinases (MNK1/2) and mTORC1 pathways modulate eIF4E activity and its inhibitor 4E-BP1.

Purpose of the Study:

  • To investigate the effect of simultaneously inhibiting MNK1/2 and PI3K/mTOR pathways on breast cancer cell migration.
  • To evaluate the efficacy of novel hybrid agents designed to inhibit both MNK1/2 and PI3K/mTOR pathways.

Main Methods:

  • Simultaneous inhibition of MNK1/2 and PI3K/mTOR signaling pathways.
  • Utilized novel, cleavable dual MNK1/2 and PI3K/mTOR inhibiting hybrid agents.
  • Assessed the rate of cell migration in breast cancer cell lines.

Main Results:

  • Simultaneous inhibition of these pathways significantly slowed breast cancer cell migration.
  • A molecular hybridization approach using novel dual-acting agents showed reduced efficacy in slowing cell migration compared to simultaneous pathway inhibition.

Conclusions:

  • Targeting both MNK1/2 and PI3K/mTOR pathways offers a potential strategy to inhibit breast cancer cell migration.
  • The design of hybrid agents may require further optimization to effectively target these combined pathways for therapeutic benefit.
Keywords:
cell signalingdual inhibitorskinasemigration

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