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Int J Oncol. 2014 Jun;44(6):1945-54. doi: 10.3892/ijo.2014.2380. Epub 2014 Apr 10.

RUVBL1 directly binds actin filaments and induces formation of cell protrusions to promote pancreatic cancer cell invasion.

Author information

1
Department of Pharmacology, School of Medicine, Kochi University, Nankoku, Kochi 783-8505, Japan.
2
Department of Pathology, School of Medicine, Kochi University, Nankoku, Kochi 783-8505, Japan.
3
Department of Gastroenterology and Hepatology, School of Medicine, Kochi University, Nankoku, Kochi 783-8505, Japan.

Abstract

We report a novel function of RUVBL1 molecule in pancreatic cancer cells. Previous reports describe that RUVBL1 belongs to the family of AAA+ ATPases that associate with chromatin-remodelling complexes and have important roles in transcriptional regulation, the DNA damage response, telomerase activity and cellular transformation. We show that knockdown of RUVBL1 inhibited the motility and invasiveness of pancreatic cancer cells. RUVBL1 localized in the cytoplasm bound filamentous actin (F-actin) in cell protrusions, and increased concentration of monomeric globular-actin (G-actin) in cell protrusions of migrating pancreatic cancer cells. Cytoplasmic RUVBL1 functioned in additional formation of actin filaments in cell protrusions. Consequently, cytoplasmic RUVBL1 contributed to the formation of membrane protrusions by promoting peripheral actin polymerization. Our results imply that these RUVBL1-actin interactions could enhance the invasive properties of pancreatic cancer cells.

PMID:
24728183
DOI:
10.3892/ijo.2014.2380
[Indexed for MEDLINE]

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