Botelho, Filomena

Gonçalves, A Cristina

Marques, Margarida

Mesquita, Luís

Neves, Sílvia S

Sarmento-Ribeiro, A Bela

Silva, Henriqueta C

Silva, Joana B

English

PubMed

Joana B Silva

S�lvia S Neves

A Gon�alves

Margarida Marques

Lu�s Mesquita

Filomena Botelho

A Sarmento-Ribeiro

Henriqueta C Silva

Springer - Publisher Connector

POSTER PRESENTATION Open Access
Evaluation of the role of mir-34b in modulation
of radioresistance in non-small cell lung cancer
Joana B Silva1,3*, Sílvia S Neves1,4, A Cristina Gonçalves1,4, Margarida Marques2,4, Luís Mesquita3,
Filomena Botelho2,4, A Bela Sarmento-Ribeiro1,4,5, Henriqueta C Silva3,4
From 16th International Charles Heidelberger Symposium on Cancer Research
Coimbra, Portugal. 26–28 September 2010
Radiotherapy is a major therapeutic weapon in
lung cancer. However, the resistance to radiotherapy is
frequent. The microRNAs of the miR-34 family, miR-
34a, miR-34b and miR-34c, described as effector mole-
cules in the cellular response to activation of P53, have
low expression levels in lung cancer [1]. The mRNA of
the anti-apoptotic protein BCL-2 is among the targets of
miR-34 family.
The aims of our study were to clarify the involvement
of miR-34b over-expression in the modulation of radia-
tion response in NSCLC cell lines and the mechanisms
involved. For these purposes we used two radioresistant
NSCLC cell lines, A549, expressing P53, and H1299, not
expressing P53. Cells transfected with pre-miR-34b or
with a transfection control were exposed to different irra-
diation doses. The response to irradiation was assessed
by cell survival curves obtained by clonogenic assay, and
flow citometry allowed the characterization of cell death
and the quantification of BCL-2, BAX and P53 protein
expression levels. Our results showed that both cell lines
had low expression levels of miR-34 family members,
especially for miR-34b/c. Over-expression of miR-34b
sensitized A549 cells to low doses of radiation and
decreased BCL-2 expression, but without changing apop-
tosis levels. H1299 cells remained unchanged.
These results suggest that in NSCLC expressing P53,
response to radiotherapy is dependent on BCL-2 levels
and may be modulated by over-expression of miRNA-
34b. Other cell death mechanisms than apoptosis, but
also involving BCL-2, like autophagy, could to be
involved.
Author details
1Department of Molecular Biology, Faculty of Medicine, University of
Coimbra (FMUC), Coimbra, Portugal. 2IBILI, FMUC, Coimbra, Portugal.
3Medical Genetics, FMUC, University of Coimbra, Coimbra, Portugal.
4CIMAGO, FMUC, Coimbra, Portugal. 5Center for Neuroscience and Cell
Biology, University of Coimbra, Portugal.
Published: 24 September 2010
Reference
1. Iorio MV, Croce CM: MicroRNAs in Cancer: Small Molecules with a Huge
Impact. J Clin Oncol 2009, 27:5848-56.
doi:10.1200/JCO.2009.24.0317
Cite this article as: Silva et al.: Evaluation of the role of mir-34b in
modulation of radioresistance in non-small cell lung cancer. BMC
Proceedings 2010 4(Suppl 2):P11.
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* Correspondence: joanabalca.silva@gmail.pt
1Department of Molecular Biology, Faculty of Medicine, University of
Coimbra (FMUC), Coimbra, Portugal
Full list of author information is available at the end of the article
Silva et al. BMC Proceedings 2010, 4(Suppl 2):P11
http://www.biomedcentral.com/1753-6561/4/S2/P11
© 2010 Silva et al; licensee BioMed Central Ltd.


Evaluation of the role of mir-34b in modulation of radioresistance in non-small cell lung cancer

CM: MicroRNAs in Cancer: Small Molecules with a Huge Impact. J Clin Oncol 2009, 27:5848-56. doi:10.1200/JCO.2009.24.0317 Cite this article as: Silva et al.: Evaluation of the role of mir-34b in modulation of radioresistance in non-small cell lung cancer.

http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=3255006

Evaluation of the role of mir-34b in modulation of radioresistance in non-small cell lung cancer

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