scholarly journals miR-34a, miR-424 and miR-513 inhibit MMSET expression to repress endometrial cancer cell invasion and sphere formation

Oncotarget ◽  
2018 ◽  
Vol 9 (33) ◽  
pp. 23253-23263 ◽  
Author(s):  
Peixin Dong ◽  
Ying Xiong ◽  
Junming Yue ◽  
Sharon J.B. Hanley ◽  
Hidemichi Watari
2020 ◽  
Vol 13 (1) ◽  
Author(s):  
Qing-an-zi Wang ◽  
Yongxiu Yang ◽  
Xiaolei Liang

Abstract Background Although lncRNA CTBP1-AS2 has been functionally analyzed only in cardiomyocyte hypertrophy and diabetes, analysis of TCGA dataset revealed its downregulation in endometrial carcinoma (EC), indicating its involvement in EC. Results In this study we found that CTBP1-AS2 was downregulated in EC and correlated with poor survival. MiR-216a might form base pairs with CTBP1-AS2 based on RNA-RNA interaction, which was confirmed by luciferase activity assay. Interestingly, upregulation of PTEN was observed after CTBP1-AS2 overexpression. Transwell assay showed that CTBP1-AS2 and PTEN overexpression led to decreased cancer cell invasion and migration and reduced enhancing effects of miR-216a on cell invasion and migration. It was known that miR-216a targeted PTEN. Conclusion Therefore, CTBP1-AS2 may sponge miR-216a to upregulate PTEN, thereby suppressing endometrial cancer cell invasion and migration.


2020 ◽  
Vol 13 (1) ◽  
Author(s):  
Qing-an-zi Wang ◽  
Yongxiu Yang ◽  
Xiaolei Liang

This article has been retracted. Please see the Retraction Notice for more detail: https://doi.org/10.1186/s13048-020-00754-0.


2014 ◽  
Vol 24 (2) ◽  
pp. 210-217 ◽  
Author(s):  
Elena Schmidt ◽  
Maike Haase ◽  
Elke Ziegler ◽  
Günter Emons ◽  
Carsten Gründker

ObjectivesThe cross talk between metastatic cancer cells and target sites is critical for the development and progression of metastases. Disruption of this interaction will allow to design mechanism-based effective and specific therapeutic interventions for metastases. We have established a coculture system of cells derived from different tumor entities and MG63 human osteoblastlike cells to analyze tumor cell invasion. Recently, we have shown that breast cancer cell invasion was dramatically increased when cocultured with MG63 cells.Using this model, we have now analyzed whether stromal-derived factor 1 (SDF-1) is responsible for human endometrial cancer cell invasion and whether kisspeptin-10 (KP-10) treatment affects SDF-1–induced invasion of endometrial cancer cells in vitro.MethodsInvasion was quantified by assessment of endometrial cancer cell migration rate through an artificial basement membrane in a modified Boyden chamber during coculture with MG63 cells or after treatment with SDF-1α, SDF-1β, or the combination of both SDF-1 isoforms. In addition, the role of SDF-1 in invasion of endometrial cancer cells was analyzed by blocking SDF-1 secretion during coculture with MG64 cells. Furthermore, the effects of KP-10 treatment on MG63 coculture-driven and SDF-1–induced invasion were analyzed.ResultsEndometrial cancer cell invasion was significantly increased when cocultured with MG63 cells. Treatment with KP-10 reduced the ability to invade a reconstituted basement membrane and to migrate in response to the cellular stimulus. This effect was significant in a dose window of 10−13 to 10−11 mol/L. During coculture, SDF-1 protein expression of MG63 cells was significantly increased. The MG63 coculture-induced increase of endometrial cancer cell invasion could be blocked by anti–SDF-1 antibodies. Treatment of endometrial cancer cells in monoculture (without MG63) with SDF-1α, SDF-1β, or the combination of both isoforms resulted in a significant increase of endometrial cancer cell invasion. The SDF-1–induced increase of endometrial cancer cell invasion was significantly reduced after treatment with KP-10.ConclusionsOur findings suggest that SDF-1 plays a major role in endometrial cancer invasion. Stromal-derived factor 1–induced invasion can be inhibited by KP-10 treatment.


2001 ◽  
Vol 82 (3) ◽  
pp. 442-449 ◽  
Author(s):  
Dong-Wook Park ◽  
Hee-Sug Ryu ◽  
Dong-Soon Choi ◽  
Young-Han Park ◽  
Ki-Hong Chang ◽  
...  

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