W Duan1, L Nian, J Qiao, N-N Liu. 1. Department of Oncology, Yan'an University Affiliated Hospital, Yan'an, China. 283132024@qq.com.
Abstract
OBJECTIVE: To illustrate the role of long non-coding RNA (lncRNA) TUG1 in the influence of the progression of cervical cancer (CC) and its underlying mechanism. PATIENTS AND METHODS: TUG1 level in CC tissues and adjacent normal ones was determined by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). Its level in CC patients with different tumor, node, and metastasis (TNM) staging and the tumor sizes were detected as well. The prognostic potential of TUG1 in CC was assessed by introducing the receiver operating characteristic (ROC) curves. The influences of TUG1 on proliferative and migratory abilities of HeLa and SiHa cells were evaluated. The subcellular distribution of TUG1 in CC cells was analyzed. Subsequently, the relative level of PUM2 (Pumilio2) in CC tissues and cell lines was examined. The prognostic potential of PUM2 in CC was assessed. RNA immunoprecipitation (RIP) and RNA pull-down were conducted to uncover the interaction between TUG1 and PUM2. Finally, the regulatory effect of TUG1/PUM2 axis on the viability of the CC cells was investigated. RESULTS: TUG1 was upregulated in CC, especially in those with worse TNM staging and larger tumor size. The overexpression of TUG1 enhanced proliferative and migratory abilities of Hela and SiHa cells. TUG1 was mainly distributed in the cytoplasm. PUM2 interacted with TUG1 and its level was positively regulated by TUG1. The silence of PUM2 reversed the promotive effect of TUG1 on the viability of the CC cells. CONCLUSIONS: TUG1 is upregulated in CC, which aggravates the progression of CC by interacting with PUM2.
OBJECTIVE: To illustrate the role of long non-coding RNA (lncRNA) TUG1 in the influence of the progression of cervical cancer (CC) and its underlying mechanism. PATIENTS AND METHODS: TUG1 level in CC tissues and adjacent normal ones was determined by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). Its level in CCpatients with different tumor, node, and metastasis (TNM) staging and the tumor sizes were detected as well. The prognostic potential of TUG1 in CC was assessed by introducing the receiver operating characteristic (ROC) curves. The influences of TUG1 on proliferative and migratory abilities of HeLa and SiHa cells were evaluated. The subcellular distribution of TUG1 in CC cells was analyzed. Subsequently, the relative level of PUM2 (Pumilio2) in CC tissues and cell lines was examined. The prognostic potential of PUM2 in CC was assessed. RNA immunoprecipitation (RIP) and RNA pull-down were conducted to uncover the interaction between TUG1 and PUM2. Finally, the regulatory effect of TUG1/PUM2 axis on the viability of the CC cells was investigated. RESULTS:TUG1 was upregulated in CC, especially in those with worse TNM staging and larger tumor size. The overexpression of TUG1 enhanced proliferative and migratory abilities of Hela and SiHa cells. TUG1 was mainly distributed in the cytoplasm. PUM2 interacted with TUG1 and its level was positively regulated by TUG1. The silence of PUM2 reversed the promotive effect of TUG1 on the viability of the CC cells. CONCLUSIONS:TUG1 is upregulated in CC, which aggravates the progression of CC by interacting with PUM2.