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Blocking the cleavage of filamin A by calpain inhibitor decreases tumor cell growth.

Journal article
Authors Reza Salimi
Sashidar Bandaru
Sevtap Gökalp
Chandu Ala
Ali Alvandian
Nilgün Yener
Levent Akyürek
Published in Anticancer research
Volume 38
Issue 4
Pages 2079-2085
ISSN 1791-7530
Publication year 2018
Published at Institute of Biomedicine, Department of Pathology
Institute of Biomedicine, Department of Medical Biochemistry and Cell Biology
Pages 2079-2085
Language en
Links dx.doi.org/10.21873/anticanres.1244...
www.ncbi.nlm.nih.gov/entrez/query.f...
Keywords Calpain, migration, proliferation, colony formation
Subject categories Medical Biotechnology (with a focus on Cell Biology (including Stem Cell Biology), Molecular Biology, Microbiology, Biochemistry or Biopharmacy), Cell and Molecular Biology, Cancer and Oncology

Abstract

Filamin A (FLNA) is the most abundant and widely expressed isoform of filamin in human tissues. It is cleaved by calpain at the hinge 1 and 2 domains, producing a 90-kDa carboxyl-terminal fragment (FLNACT). Recently, it has been shown that FLNACTmediates cell signaling and transports transcription factors into the cell nucleus. However, the significance of cleavage of FLNA by calpain has not been studied in cancer cell growth. Calpeptin is a chemical inhibitor of both calpain 1 and 2 that cleaves FLNA. In this study, we questioned if inhibiting calpain using calpeptin would decrease tumor cell proliferation, migration, invasion, and colony formation.Human melanoma (A7), prostate cancer (PC3), mouse fibrosarcoma (T241) and endothelial (MS1) cells were assayed for proliferation, migration, invasion and colony formation after treatment with calpeptin. Cell lysates were immunoblotted for FLNA and FLNACTResults: Calpeptin treatment of these cells resulted in a decreased production of FLNACTCalpeptin-treated human and mouse tumor cells displayed impaired proliferation, migration, and colony formation.These data suggest that the cleavage of FLNA by calpain is an important cellular event in the regulation of tumor cell growth.

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