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

Mijung Kwon, Steven K. Libutti

Research output: Contribution to journalArticle

5 Citations (Scopus)

Abstract

Introduction: Filamin A interacting protein 1-like (FILIP1L) is a novel tumor suppressor-like protein that has its expression downregulated in various cancers through promoter hypermethylation. When overexpressed, FILIP1L inhibits cancer cell invasion and metastasis through the inhibition of canonical WNT signaling. Areas covered: This review gives an overview of the structure and isoforms, gene expression and cellular location of FILIP1L, and how FILIP1L inhibits cancer invasion and metastasis. Furthermore, the review discusses the potential mechanism by which FILIP1L inhibits cancer metastasis through inhibiting canonical WNT signaling and thus blocking downstream β-catenin transcriptional targets. Expert opinion: By inhibiting β-catenin, the key transcriptional factor of the canonical WNT signaling pathway, FILIP1L could block various downstream pathways that are regulated by β-catenin transcriptional targets. FILIP1L could therefore have great potential as a novel cancer therapeutic target. However, in order to fulfill its therapeutic potential, its precise mechanism of action of antimetastatic activity has to be identified. In addition, the physiological role of FILIP1L and its relationship with other isoforms needs to be characterized.

Original languageEnglish (US)
Pages (from-to)1435-1447
Number of pages13
JournalExpert Opinion on Therapeutic Targets
Volume18
Issue number12
DOIs
StatePublished - Dec 1 2014

Fingerprint

Filamins
Catenins
Neoplasms
Proteins
Therapeutics
Neoplasm Metastasis
Protein Isoforms
Tumor Suppressor Proteins
Expert Testimony
Gene expression
Tumors
Down-Regulation
Cells
Gene Expression

Keywords

  • Epithelial-to-mesenchymal transition
  • Filamin A interacting protein 1-like
  • Invasion
  • Metastasis
  • MMP
  • Ovarian cancer
  • Pancreatic cancer
  • WNT signaling
  • β-catenin degradation

ASJC Scopus subject areas

  • Drug Discovery
  • Pharmacology
  • Clinical Biochemistry
  • Molecular Medicine

Cite this

Filamin A interacting protein 1-like as a therapeutic target in cancer. / Kwon, Mijung; Libutti, Steven K.

In: Expert Opinion on Therapeutic Targets, Vol. 18, No. 12, 01.12.2014, p. 1435-1447.

Research output: Contribution to journalArticle

Kwon, Mijung ; Libutti, Steven K. / Filamin A interacting protein 1-like as a therapeutic target in cancer. In: Expert Opinion on Therapeutic Targets. 2014 ; Vol. 18, No. 12. pp. 1435-1447.
@article{b988fa64d6fa40a58db4de4da5acbe84,
title = "Filamin A interacting protein 1-like as a therapeutic target in cancer",
abstract = "Introduction: Filamin A interacting protein 1-like (FILIP1L) is a novel tumor suppressor-like protein that has its expression downregulated in various cancers through promoter hypermethylation. When overexpressed, FILIP1L inhibits cancer cell invasion and metastasis through the inhibition of canonical WNT signaling. Areas covered: This review gives an overview of the structure and isoforms, gene expression and cellular location of FILIP1L, and how FILIP1L inhibits cancer invasion and metastasis. Furthermore, the review discusses the potential mechanism by which FILIP1L inhibits cancer metastasis through inhibiting canonical WNT signaling and thus blocking downstream β-catenin transcriptional targets. Expert opinion: By inhibiting β-catenin, the key transcriptional factor of the canonical WNT signaling pathway, FILIP1L could block various downstream pathways that are regulated by β-catenin transcriptional targets. FILIP1L could therefore have great potential as a novel cancer therapeutic target. However, in order to fulfill its therapeutic potential, its precise mechanism of action of antimetastatic activity has to be identified. In addition, the physiological role of FILIP1L and its relationship with other isoforms needs to be characterized.",
keywords = "Epithelial-to-mesenchymal transition, Filamin A interacting protein 1-like, Invasion, Metastasis, MMP, Ovarian cancer, Pancreatic cancer, WNT signaling, β-catenin degradation",
author = "Mijung Kwon and Libutti, {Steven K.}",
year = "2014",
month = "12",
day = "1",
doi = "10.1517/14728222.2014.957181",
language = "English (US)",
volume = "18",
pages = "1435--1447",
journal = "Expert Opinion on Therapeutic Targets",
issn = "1472-8222",
publisher = "Informa Healthcare",
number = "12",

}

TY - JOUR

T1 - Filamin A interacting protein 1-like as a therapeutic target in cancer

AU - Kwon, Mijung

AU - Libutti, Steven K.

PY - 2014/12/1

Y1 - 2014/12/1

N2 - Introduction: Filamin A interacting protein 1-like (FILIP1L) is a novel tumor suppressor-like protein that has its expression downregulated in various cancers through promoter hypermethylation. When overexpressed, FILIP1L inhibits cancer cell invasion and metastasis through the inhibition of canonical WNT signaling. Areas covered: This review gives an overview of the structure and isoforms, gene expression and cellular location of FILIP1L, and how FILIP1L inhibits cancer invasion and metastasis. Furthermore, the review discusses the potential mechanism by which FILIP1L inhibits cancer metastasis through inhibiting canonical WNT signaling and thus blocking downstream β-catenin transcriptional targets. Expert opinion: By inhibiting β-catenin, the key transcriptional factor of the canonical WNT signaling pathway, FILIP1L could block various downstream pathways that are regulated by β-catenin transcriptional targets. FILIP1L could therefore have great potential as a novel cancer therapeutic target. However, in order to fulfill its therapeutic potential, its precise mechanism of action of antimetastatic activity has to be identified. In addition, the physiological role of FILIP1L and its relationship with other isoforms needs to be characterized.

AB - Introduction: Filamin A interacting protein 1-like (FILIP1L) is a novel tumor suppressor-like protein that has its expression downregulated in various cancers through promoter hypermethylation. When overexpressed, FILIP1L inhibits cancer cell invasion and metastasis through the inhibition of canonical WNT signaling. Areas covered: This review gives an overview of the structure and isoforms, gene expression and cellular location of FILIP1L, and how FILIP1L inhibits cancer invasion and metastasis. Furthermore, the review discusses the potential mechanism by which FILIP1L inhibits cancer metastasis through inhibiting canonical WNT signaling and thus blocking downstream β-catenin transcriptional targets. Expert opinion: By inhibiting β-catenin, the key transcriptional factor of the canonical WNT signaling pathway, FILIP1L could block various downstream pathways that are regulated by β-catenin transcriptional targets. FILIP1L could therefore have great potential as a novel cancer therapeutic target. However, in order to fulfill its therapeutic potential, its precise mechanism of action of antimetastatic activity has to be identified. In addition, the physiological role of FILIP1L and its relationship with other isoforms needs to be characterized.

KW - Epithelial-to-mesenchymal transition

KW - Filamin A interacting protein 1-like

KW - Invasion

KW - Metastasis

KW - MMP

KW - Ovarian cancer

KW - Pancreatic cancer

KW - WNT signaling

KW - β-catenin degradation

UR - http://www.scopus.com/inward/record.url?scp=84964225075&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84964225075&partnerID=8YFLogxK

U2 - 10.1517/14728222.2014.957181

DO - 10.1517/14728222.2014.957181

M3 - Article

C2 - 25200207

AN - SCOPUS:84964225075

VL - 18

SP - 1435

EP - 1447

JO - Expert Opinion on Therapeutic Targets

JF - Expert Opinion on Therapeutic Targets

SN - 1472-8222

IS - 12

ER -