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Ionizing radiation differentially modulates Wnt pathway components through ILK in normal and tumor bone cell lineages
Author(s) -
Naves Marcelo Andery,
NogueiraPedro Amanda,
Peres Giovani B.,
Giordani Adelmo,
Segreto Helena,
Teixeira Vicente P.C.
Publication year - 2013
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.27.1_supplement.lb434
Subject(s) - wnt signaling pathway , viability assay , apoptosis , protein kinase b , cell growth , flow cytometry , microbiology and biotechnology , pi3k/akt/mtor pathway , signal transduction , chemistry , biology , cancer research , biochemistry
Osteosarcoma (OS) frequently invades, mestastasizes, relapses and is characteristically radioresistent. Integrin‐linked kinase (ILK) modulates cell survival, death and radiosensibility. It can also interact with Wnt signaling pathway that is essential to skeletal development and may also play an important role in OS progression. Murine pre‐osteoblast (MC3T3‐E1), rat OS (UMR‐106) and human OS (MG63) lineages were irradiated using a 60Co radiation source (2 and 6 Gy for 24 e 72 hr). We analyzed cell viability (MTT assay), adhesion (crystal violet assay), apoptosis, ILK, βcatenin, p‐GSK‐3β and p‐Akt protein expression (flow cytometry) and gelatinolytic activity (zymography). Osteoblastic cells presented a substantial decrease in viability and cell adhesion. Apoptosis was reduced in MC3T3 groups irradiated with 6Gy dose. OS cells were less viable (except MG63 cells at 24 hr) and less adherent. Apoptosis increased in irradiated groups. ILK, p‐GSK‐3β, β‐catenin and p‐Akt expressions were significantly increased in all irradiated cell lineages, except in MC3T3 cells treated for 72 hr that showed a decrease in those protein expressions. Irradiation didn't modify cell gelatinolytic activity. Ionizing radiation differentially modulated the cellular biology aspects of osteoblasts and OS lineages. This was probably accomplished by modulation of canonical Wnt signaling pathway through ILK.