Nesprin-1 impact on tumorigenic cell phenotypes

Nesprin-1 impact on tumorigenic cell phenotypes

The largest protein of the nuclear envelope (NE) is Nesprin-1 which forms a network along the NE interacting with actin, Emerin, Lamin, and SUN proteins. Mutations in the SYNE1 gene and reduction in Nesprin-1 protein levels have been reported to correlate with several age related diseases and cancer...

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Bibliographic Details
Published in:Molecular biology reports Vol. 47; no. 2; pp. 921 - 934
Main Authors: Sur-Erdem, Ilknur, Hussain, Muhammed Sajid, Asif, Maria, Pınarbası, Nareg, Aksu, Ali Cenk, Noegel, Angelika A.
Format: Journal Article
Language:English
Published: Dordrecht Springer Netherlands 01-02-2020
Springer Nature B.V
Subjects:
Actin
Actins - genetics
Actins - metabolism
Animal Anatomy
Animal Biochemistry
Biomedical and Life Sciences
Carcinogenesis - genetics
Carcinogenesis - metabolism
Cell Line, Tumor
Cell Nucleus - metabolism
Cytoskeletal Proteins - genetics
Cytoskeletal Proteins - metabolism
DNA damage
Ectopic expression
Gene Expression - genetics
Gene Expression Regulation, Neoplastic - genetics
Genomes
Hepatocytes
Histology
Humans
Life Sciences
Liver cancer
Localization
Microfilament Proteins - metabolism
Morphology
Mutation
Nerve Tissue Proteins - genetics
Nerve Tissue Proteins - metabolism
Nuclear Envelope - genetics
Nuclear Envelope - metabolism
Original Article
Phenotype
Phenotypes
Proteins
Senescence
Nesprin-1
Genome stability
Nuclear envelope
Cellular senescence
Cancer
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Summary:The largest protein of the nuclear envelope (NE) is Nesprin-1 which forms a network along the NE interacting with actin, Emerin, Lamin, and SUN proteins. Mutations in the SYNE1 gene and reduction in Nesprin-1 protein levels have been reported to correlate with several age related diseases and cancer. In the present study, we tested whether Nesprin-1 overexpression can reverse the malignant phenotype of Huh7 cells, a human liver cancer cell line, which carries a mutation in the SYNE1 gene resulting in reduced Nesprin-1 protein levels, has altered nuclear shape, altered amounts and localization of NE components, centrosome localization and genome stability. Ectopic expression of a mini-Nesprin-1 led to an improvement of the nuclear shape, corrected the mislocalization of NE proteins, the centrosome positioning, and the alterations in the DNA damage response network. Additionally, Nesprin-1 had a profound effect on cellular senescence. These findings suggest that Nesprin-1 may be effective in tumorigenic cell phenotype correction of human liver cancer.
ISSN:0301-4851
1573-4978
DOI:10.1007/s11033-019-05184-w