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Overexpression of long non-coding RNA TUG1 predicts poor prognosis and promotes cancer cell proliferation and migration in high-grade muscle-invasive bladder cancer

R. Iliev, R. Kleinova, J. Juracek, J. Dolezel, Z. Ozanova, M. Fedorko, D. Pacik, M. Svoboda, M. Stanik, O. Slaby,

. 2016 ; 37 (10) : 13385-13390. [pub] 20160727

Jazyk angličtina Země Spojené státy americké

Typ dokumentu časopisecké články

Perzistentní odkaz   https://www.medvik.cz/link/bmc17013635

Grantová podpora
NV15-31071A MZ0 CEP - Centrální evidence projektů

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.

Citace poskytuje Crossref.org

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$a Long non-coding RNA TUG1 is involved in the development and progression of a variety of tumors. Little is known about TUG1 function in high-grade muscle-invasive bladder cancer (MIBC). The aims of our study were to determine expression levels of long non-coding RNA TUG1 in tumor tissue, to evaluate its relationship with clinico-pathological features of high-grade MIBC, and to describe its function in MIBC cells in vitro. TUG1 expression levels were determined in paired tumor and adjacent non-tumor bladder tissues of 47 patients with high-grade MIBC using real-time PCR. Cell line T-24 and siRNA silencing were used to study the TUG1 function in vitro. We observed significantly increased levels of TUG1 in tumor tissue in comparison to adjacent non-tumor bladder tissue (P < 0.0001). TUG1 levels were significantly increased in metastatic tumors (P = 0.0147) and were associated with shorter overall survival of MIBC patients (P = 0.0241). TUG1 silencing in vitro led to 34 % decrease in cancer cell proliferation (P = 0.0004) and 23 % reduction in migration capacity of cancer cells (P < 0.0001). We did not observe any significant effects of TUG1 silencing on cell cycle distribution and number of apoptotic cells. Our study confirmed overexpression of TUG1 in MIBC tumor tissue and described its association with worse overall survival in high-grade MIBC patients. Together with in vitro observations, these data suggest an oncogenic role of TUG1 and its potential usage as biomarker or therapeutic target in MIBC.
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$a Kleinova, Renata $u Central European Institute of Technology (CEITEC), Masaryk University, University Campus Bohunice, Building A35, Room 217, Kamenice 5, 625 00, Brno, Czech Republic.
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$a Juracek, Jaroslav $u Central European Institute of Technology (CEITEC), Masaryk University, University Campus Bohunice, Building A35, Room 217, Kamenice 5, 625 00, Brno, Czech Republic. Department of Comprehensive Cancer Care, Masaryk Memorial Cancer Institute, Zluty kopec 7, Brno, Czech Republic.
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$a Dolezel, Jan $u Department of Urologic Oncology, Masaryk Memorial Cancer Institute, Zluty kopec 7, 656 53, Brno, Czech Republic.
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$a Fedorko, Michal $u Department of Urology, University Hospital Brno and Masaryk University Brno, Jihlavska 20, 62500, Brno, Czech Republic.
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$a Svoboda, Marek $u Central European Institute of Technology (CEITEC), Masaryk University, University Campus Bohunice, Building A35, Room 217, Kamenice 5, 625 00, Brno, Czech Republic. Department of Comprehensive Cancer Care, Masaryk Memorial Cancer Institute, Zluty kopec 7, Brno, Czech Republic.
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$a Stanik, Michal $u Department of Urologic Oncology, Masaryk Memorial Cancer Institute, Zluty kopec 7, 656 53, Brno, Czech Republic. stanik@mou.cz.
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$a Slaby, Ondrej $u Central European Institute of Technology (CEITEC), Masaryk University, University Campus Bohunice, Building A35, Room 217, Kamenice 5, 625 00, Brno, Czech Republic. on.slaby@gmail.com. Department of Comprehensive Cancer Care, Masaryk Memorial Cancer Institute, Zluty kopec 7, Brno, Czech Republic. on.slaby@gmail.com.
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