Overexpression of long non-coding RNA TUG1 predicts poor prognosis and promotes cancer cell proliferation and migration in high-grade muscle-invasive bladder cancer
Jazyk angličtina Země Spojené státy americké Médium print-electronic
Typ dokumentu časopisecké články
PubMed
27460088
DOI
10.1007/s13277-016-5177-9
PII: 10.1007/s13277-016-5177-9
Knihovny.cz E-zdroje
- Klíčová slova
- Long non-coding RNA, Migration, Muscle-invasive bladder cancer, Prognosis, Proliferation, TUG1,
- MeSH
- apoptóza MeSH
- buněčný cyklus MeSH
- invazivní růst nádoru MeSH
- kvantitativní polymerázová řetězová reakce MeSH
- lidé MeSH
- malá interferující RNA genetika MeSH
- messenger RNA genetika MeSH
- nádorové biomarkery genetika MeSH
- nádorové buňky kultivované MeSH
- nádory močového měchýře genetika patologie MeSH
- nádory svalů genetika patologie MeSH
- pohyb buněk * MeSH
- polymerázová řetězová reakce s reverzní transkripcí MeSH
- prognóza MeSH
- progrese nemoci MeSH
- proliferace buněk * MeSH
- regulace genové exprese u nádorů * MeSH
- RNA dlouhá nekódující antagonisté a inhibitory genetika MeSH
- staging nádorů MeSH
- Check Tag
- lidé MeSH
- ženské pohlaví MeSH
- Publikační typ
- časopisecké články MeSH
- Názvy látek
- malá interferující RNA MeSH
- messenger RNA MeSH
- nádorové biomarkery MeSH
- RNA dlouhá nekódující MeSH
- TUG1 long noncoding RNA, human MeSH Prohlížeč
Long non-coding RNA TUG1 is involved in the development and progression of a variety of tumors. Little is known about TUG1 function in high-grade muscle-invasive bladder cancer (MIBC). The aims of our study were to determine expression levels of long non-coding RNA TUG1 in tumor tissue, to evaluate its relationship with clinico-pathological features of high-grade MIBC, and to describe its function in MIBC cells in vitro. TUG1 expression levels were determined in paired tumor and adjacent non-tumor bladder tissues of 47 patients with high-grade MIBC using real-time PCR. Cell line T-24 and siRNA silencing were used to study the TUG1 function in vitro. We observed significantly increased levels of TUG1 in tumor tissue in comparison to adjacent non-tumor bladder tissue (P < 0.0001). TUG1 levels were significantly increased in metastatic tumors (P = 0.0147) and were associated with shorter overall survival of MIBC patients (P = 0.0241). TUG1 silencing in vitro led to 34 % decrease in cancer cell proliferation (P = 0.0004) and 23 % reduction in migration capacity of cancer cells (P < 0.0001). We did not observe any significant effects of TUG1 silencing on cell cycle distribution and number of apoptotic cells. Our study confirmed overexpression of TUG1 in MIBC tumor tissue and described its association with worse overall survival in high-grade MIBC patients. Together with in vitro observations, these data suggest an oncogenic role of TUG1 and its potential usage as biomarker or therapeutic target in MIBC.
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