Medizinische Universität Graz Austria/Österreich - Forschungsportal - Medical University of Graz
Gewählte Publikation:
SHR Neuro Krebs Kardio Lipid Stoffw Microb
Froehlich, EV; Rinner, B; Deutsch, AJ; Meditz, K; Knausz, H; Troppan, K; Scheipl, S; Wibmer, C; Leithner, A; Liegl, B; Lohberger, B.
Examination of survivin expression in 50 chordoma specimens--A histological and in vitro study.
J Orthop Res. 2015; 33(5):771-778
Doi: 10.1002/jor.22819
[OPEN ACCESS]
Web of Science
PubMed
FullText
FullText_MUG
- Führende Autor*innen der Med Uni Graz
- Fröhlich-Sorger Elke Verena
- Rinner Beate
- Co-Autor*innen der Med Uni Graz
- Deutsch Alexander
- Knausz Heike
- Leithner Andreas
- Liegl-Atzwanger Bernadette
- Lohberger Birgit
- Meditz Katharina
- Prochazka Katharina
- Scheipl Susanne
- Wibmer Christine Linda
- Altmetrics:
- Dimensions Citations:
- Plum Analytics:
- Scite (citation analytics):
- Abstract:
- Chordomas mainly arise along the axial skeleton and are characterized by their slow but destructive growth. Prognosis and quality of life are poor because treatment options are mainly limited to surgery and radiotherapy. Survivin, a member of the apoptosis inhibitor protein family, functions as a key regulator of mitosis and programmed cell death, and is overexpressed in many tumor types. The aim of this study was to determine the role of survivin in chordomas. Survivin expression was investigated in 50 chordoma samples and three chordoma cell lines using immunohistochemistry. The intensity of immunostaining was evaluated in regard to the development of recurrences. The immunohistochemical results were correlated with clinical parameters like gender, age, tumor size, and location and were performed in primary chordomas as well as in recurrent lesions. Furthermore, survivin knockdown experiments on chordoma cell lines were performed. YM155 decreased the growth behavior of chordoma cells dose- and time dependently. Transient knockdown of survivin led to a G2/M arrest, decreased proliferation, consistently induced an increase of polyploidy and morphological changes, and induced apoptosis. The resultant data from this study suggest that survivin plays a cell cycle-progressive role in chordomas. Hence, regulation of survivin by YM155 is a promising new target for the development of new therapeutic drugs. © 2015 Orthopaedic Research Society. Published by Wiley Periodicals, Inc.
- Find related publications in this database (using NLM MeSH Indexing)
- Adult -
- Aged -
- Aged, 80 and over -
- Apoptosis - drug effects
- Cell Cycle - drug effects
- Cell Line, Tumor -
- Chordoma - drug therapy
- Chordoma - metabolism
- Drug Screening Assays, Antitumor -
- Female -
- Humans -
- Imidazoles - pharmacology
- Imidazoles - therapeutic use
- Immunohistochemistry -
- Inhibitor of Apoptosis Proteins - antagonists & inhibitors
- Inhibitor of Apoptosis Proteins - metabolism
- Male -
- Middle Aged -
- Naphthoquinones - pharmacology
- Naphthoquinones - therapeutic use
- Neoplasm Recurrence, Local - metabolism
- RNA, Small Interfering -
- Retrospective Studies -
- Skull Neoplasms - metabolism
- Spinal Neoplasms - metabolism
- Survivin -
- Young Adult -
- Find related publications in this database (Keywords)
- chordoma
- survivin
- YM155
- cell cycle