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Filamin A interacting protein 1-like as a therapeutic target in cancer

Mijung Kwon1, Steven K Libutti

  • 1Albert Einstein College of Medicine of Yeshiva University, Department of Surgery , Bronx, NY 10461 , USA.

Expert Opinion on Therapeutic Targets
|September 10, 2014
PubMed
Abstract

Insights

Filamin A interacting protein 1-like (FILIP1L) suppresses cancer metastasis by inhibiting WNT signaling and beta-catenin. Further research is needed to fully understand FILIP1L

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Research

Background:

  • Filamin A interacting protein 1-like (FILIP1L) is a novel tumor suppressor-like protein.
  • FILIP1L expression is downregulated in various cancers via promoter hypermethylation.
  • Overexpressed FILIP1L inhibits cancer cell invasion and metastasis by suppressing canonical WNT signaling.

Purpose of the Study:

  • To review the structure, isoforms, gene expression, and cellular location of FILIP1L.
  • To elucidate how FILIP1L inhibits cancer invasion and metastasis.
  • To discuss the mechanism by which FILIP1L inhibits metastasis via WNT signaling and beta-catenin.

Main Methods:

  • Literature review of FILIP1L's role in cancer.
  • Analysis of FILIP1L's interaction with WNT signaling pathway.
  • Examination of FILIP1L's effect on beta-catenin transcriptional targets.

Main Results:

  • FILIP1L inhibits cancer cell invasion and metastasis.
  • FILIP1L suppresses canonical WNT signaling.
  • FILIP1L blocks downstream beta-catenin transcriptional targets.

Conclusions:

  • FILIP1L inhibits beta-catenin, a key factor in WNT signaling, thus blocking downstream pathways.
  • FILIP1L shows potential as a novel therapeutic target for cancer.
  • Further research is required to identify FILIP1L's precise antimetastatic mechanism and physiological role.
Keywords:
MMPWNT signalingepithelial-to-mesenchymal transitionfilamin A interacting protein 1-likeinvasionmetastasisovarian cancerpancreatic cancerβ-catenin degradation

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