The lncRNA CCAT1 upregulates TGFβR1 via sponging miR-490-3p to promote TGFβ1-induced EMT of ovarian cancer cells

Ovarian cancer is the fifth leading cause of cancer deaths in women worldwide. was reported to play a critical role in cell metastasis of ovarian cancer. However, little is known about the detailed mechanism of how enhances TGFβ1-induced EMT of ovarian cancer cells. We used RT-qPCR to examine the le...

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Veröffentlicht in:Cancer cell international 2018-09, Vol.18 (1), p.145-145, Article 145
Hauptverfasser: Mu, Yang, Li, Na, Cui, Yu-Lan
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Sprache:eng
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Zusammenfassung:Ovarian cancer is the fifth leading cause of cancer deaths in women worldwide. was reported to play a critical role in cell metastasis of ovarian cancer. However, little is known about the detailed mechanism of how enhances TGFβ1-induced EMT of ovarian cancer cells. We used RT-qPCR to examine the level of - - and and western blot to detect the protein level of TGFβR1 and EMT-associated markers. We utilized luciferase reporter assay to confirm the direct interaction of or TGFβ1 with - - . Wound healing and invasion assay were employed to investigate the role of and - - in the TGFβ1-induced migration and cell invasion of ovarian cancer cells, respectively. TGFβ1 stimulated the expression of CCAT1. And CC knockdown decreased cell migration, invasion and EMT-associated markers expression of ovarian cancer cells treated with TGFβ1. directly targeted and downregulated - - , then increasing TGFβR1 level. - - was shown to regulate cell invasion, migration and EMT markers expression via TGFβR1. In addition, we also observed that - - was essential for TGFβ1-induced tumor cell invasion and migration influenced by . level was significantly higher in tumors than adjacent normal tissue, in contrast, - - level was lower in ovarian tumors. Here, we reveal that contributes to TGFβ1-induced EMT of ovarian tumor cells through - - /TGFR1 axis. These findings will provide deep insights into the mechanism by which exerts its oncogenic role in ovarian cancer progression and facilitate developing novel therapeutical therapies for treating ovarian cancer.
ISSN:1475-2867
1475-2867
DOI:10.1186/s12935-018-0604-1