These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: Silencing the long noncoding RNA, TINCR, a molecular sponge of miR‑335, inhibits the malignant phenotype of epithelial ovarian cancer via FGF2 suppression.
    Author: Li R, Wang Y, Xu Y, He X, Li Y.
    Journal: Int J Oncol; 2019 Nov; 55(5):1110-1124. PubMed ID: 31545411.
    Abstract:
    Aberrant terminal differentiation‑induced noncoding RNA (TINCR) expression has been identified in multiple human cancer types and is functionally significant in cancer progression. However, to the best of our knowledge, no reported studies have investigated the expression pattern and precise role of TINCR in epithelial ovarian cancer (EOC). Here, TINCR expression levels in EOC tissues and cell lines were determined by reverse transcription‑quantitative polymerase chain reaction. Cell Counting Kit‑8 assays, flow cytometric analysis, Transwell migration and invasion assays, and in vivo xenograft experiments were performed to determine the influence of TINCR on the malignant phenotype of EOC cells in vitro and in vivo. The molecular mechanisms associated with the tumor‑promoting roles of TINCR during EOC progression were elucidated using a series of experiments. TINCR expression was higher in EOC tissues and cell lines compared with normal cells. An analysis of the association between TINCR expression and clinicopathological characteristics showed that increased TINCR expression was closely related to tumor size, FIGO stage, and lymphatic metastasis. In addition, the overall survival rates of EOC patients with high TINCR expression levels were lower than in those with low TINCR expression levels. Functional experiments showed that TINCR deficiency attenuated the proliferation, migration, and invasion of EOC cells in vitro and hindered EOC tumor growth in vivo. In addition, EOC cell apoptosis increased after TINCR knockdown. Mechanistically, TINCR was shown to function as a sponge of microRNA‑335 (miR‑335) in EOC cells, thereby regulating fibroblast growth factor 2 (FGF2) expression. miR‑335 inhibition partially counteracted the effect of TINCR knockdown on the aggressive behavior of EOC cells. This study showed, for the first time to the best of our knowledge, that silencing TINCR, which interacts with miR‑335, inhibited EOC progression in vitro and in vivo by decreasing FGF2 expression. Hence, this lncRNA could be a potential prognostic biomarker and effective target for therapeutic intervention in EOC.
    [Abstract] [Full Text] [Related] [New Search]