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Cancer Cell International
Published in: Cancer Cell International 1/2013

Open Access 01-12-2013 | Primary research

Low-dose etoposide-treatment induces endoreplication and cell death accompanied by cytoskeletal alterations in A549 cells: Does the response involve senescence? The possible role of vimentin

Authors: Anna Litwiniec, Lidia Gackowska, Anna Helmin-Basa, Agnieszka Żuryń, Alina Grzanka

Published in: Cancer Cell International | Issue 1/2013

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Abstract

Background

Senescence in the population of cells is often described as a program of restricted proliferative capacity, which is manifested by broad morphological and biochemical changes including a metabolic shift towards an autophagic-like response and a genotoxic-stress related induction of polyploidy. Concomitantly, the cell cycle progression of a senescent cell is believed to be irreversibly arrested. Recent reports suggest that this phenomenon may have an influence on the therapeutic outcome of anticancer treatment. The aim of this study was to verify the possible involvement of this program in the response to the treatment of the A549 cell population with low doses of etoposide, as well as to describe accompanying cytoskeletal alterations.

Methods

After treatment with etoposide, selected biochemical and morphological parameters were examined, including: the activity of senescence-associated ß-galactosidase, SAHF formation, cell cycle progression, the induction of p21Cip1/Waf1/Sdi1 and cyclin D1, DNA strand breaks, the disruption of cell membrane asymmetry/integrity and ultrastructural alterations. Vimentin and G-actin cytoskeleton was evaluated both cytometrically and microscopically.

Results and conclusions

Etoposide induced a senescence-like phenotype in the population of A549 cells. Morphological alterations were nevertheless not directly coupled with other senescence markers including a stable cell cycle arrest, SAHF formation or p21Cip1/Waf1/Sdi1 induction. Instead, a polyploid, TUNEL-positive fraction of cells visibly grew in number. Also upregulation of cyclin D1 was observed. Here we present preliminary evidence, based on microscopic analyses, that suggest a possible role of vimentin in nuclear alterations accompanying polyploidization-depolyploidization events following genotoxic insults.
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Metadata
Title
Low-dose etoposide-treatment induces endoreplication and cell death accompanied by cytoskeletal alterations in A549 cells: Does the response involve senescence? The possible role of vimentin
Authors
Anna Litwiniec
Lidia Gackowska
Anna Helmin-Basa
Agnieszka Żuryń
Alina Grzanka
Publication date
01-12-2013
Publisher
BioMed Central
Published in
Cancer Cell International / Issue 1/2013
Electronic ISSN: 1475-2867
DOI
https://doi.org/10.1186/1475-2867-13-9

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Cancer Cell International 1/2013 Go to the issue

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MEK inhibition induced downregulation of MRP1 and MRP3 expression in experimental hepatocellular carcinoma

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Anti-cancer effects of ginsenoside compound k on pediatric acute myeloid leukemia cells

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PI3-kinase inhibition synergistically promoted the anti-tumor effect of lupeol in hepatocellular carcinoma

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Independent of ErbB1 gene copy number, EGF stimulates migration but is not associated with cell proliferation in non-small cell lung cancer

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Erratum to: Functional disruption of macrophage migration inhibitory factor (MIF) suppresses proliferation of human h460 lung cancer cells by caspase-dependent apoptosis

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Expression patterns of Phf5a/PHF5A and Gja1/GJA1 in rat and human endometrial cancer
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