4.3 Article

Downregulation of the long noncoding RNA TUG1 inhibits the proliferation, migration, invasion and promotes apoptosis of renal cell carcinoma

期刊

JOURNAL OF MOLECULAR HISTOLOGY
卷 47, 期 4, 页码 421-428

出版社

SPRINGER
DOI: 10.1007/s10735-016-9683-2

关键词

TUG1; Renal cell carcinoma; siRNA-TUG1; Biomarker

资金

  1. Young Scientists Fund of the National Natural Science Foundation of China [81502207, 81201579, 81301740]
  2. Shenzhen Basic Research Project [JCYJ20130401114928183, JCYJ20140416180323426]
  3. Shenzhen Knowledge Innovation Project [JCYJ20130401114715714]
  4. Project of Science and Technology of Shenzhen (Technological Innovation Project) [CXZZ20120614154434310]
  5. Plan of the Construction of Innovative Environment in Shenzhen (Key Laboratory) [ZDSY20130531165409949]

向作者/读者索取更多资源

Long non-coding RNAs, a newly discovered category of noncoding genes, play a leading role in various biological processes, including tumorigenesis. In our study, we aimed to examine the TUG1 expression, and explore the influence of TUG1 silencing on cell proliferation and apoptosis in renal cell carcinoma (RCC) cell lines. The TUG1 expression level was detected using quantitative real-time PCR reverse transcription-polymerase chain reaction in 40 paired clear cell renal cell carcinoma (ccRCC) and adjacent paired normal tissues, as well as four RCC cell lines and one normal human proximal tubule epithelial cell line HK-2. Small interfering RNA was applied to suppress the TUG1 expression in RCC cell lines (A489 and A704). In vitro assays were conducted to further deliberate its potential functions in RCC progression. The relative TUG1 expression was significantly higher in ccRCC tissues compared to the adjacent normal renal tissues. In addition, higher TUG1 expression was equally detected in RCC cell lines (particularly in A498 and A704) compared to HK-2. The ccRCC specimens with higher TUG1 expression had a higher Fuhrman grade and larger tumor size than those with lower TUG1 expression. In vitro assays results suggested that knockdown of TUG1 suppressed RCC cells migration, invasion and proliferation, while the apoptosis process was activated. Our results indicate that TUG1 is identified as a novel oncogene in the morbid state of RCC, which potentially acts as a therapeutic target/biomarker in RCC. [GRAPHICS] .

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