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

Artikel i vetenskaplig tidskrift
Författare Reza Salimi
Sashidar Bandaru
Sravani Devarakonda
Sevtap Gökalp
Chandu Ala
Ali Alvandian
Nilgün Yener
Levent Akyürek
Publicerad i Anticancer Research
Volym 38
Nummer/häfte 4
Sidor 2079-2085
ISSN 0250-7005
Publiceringsår 2018
Publicerad vid Institutionen för biomedicin, avdelningen för medicinsk kemi och cellbiologi
Sidor 2079-2085
Språk en
Ämnesord Calpain, migration, proliferation, colony formation
Ämneskategorier Cancer och onkologi, Cell- och molekylärbiologi, Medicinsk bioteknologi (med inriktning mot cellbiologi (inklusive stamcellsbiologi), molekylärbiologi, mikrobiologi, biokemi eller biofarmaci)

Sammanfattning

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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