Localization of Matrix Metalloproteinases on Endometrial Cancer Cell Invasion in Vitro

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

scholarly journals RETRACTED ARTICLE: LncRNA CTBP1-AS2 sponges miR-216a to upregulate PTEN and suppress endometrial cancer cell invasion and migration

2020 ◽  
Vol 13 (1) ◽  
Author(s):  
Qing-an-zi Wang ◽  
Yongxiu Yang ◽  
Xiaolei Liang
Keyword(s):  
Endometrial Cancer ◽  
Cancer Cell ◽  
Cell Invasion ◽  
Cardiomyocyte Hypertrophy ◽  
Cancer Cell Invasion ◽  
Endometrial Cancer Cell ◽  
Invasion And Migration ◽  
Tcga Dataset ◽  
And Migration ◽  
Rna Interaction

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.

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
Keyword(s):  
Endometrial Cancer ◽  
Cancer Cell ◽  
Cell Invasion ◽  
Cancer Cell Invasion ◽  
Endometrial Cancer Cell ◽  
Sphere Formation

scholarly journals Retraction Note: LncRNA CTBP1-AS2 sponges miR-216a to upregulate PTEN and suppress endometrial cancer cell invasion and migration

2020 ◽  
Vol 13 (1) ◽  
Author(s):  
Qing-an-zi Wang ◽  
Yongxiu Yang ◽  
Xiaolei Liang
Keyword(s):  
Endometrial Cancer ◽  
Cancer Cell ◽  
Cell Invasion ◽  
Cancer Cell Invasion ◽  
Endometrial Cancer Cell ◽  
Invasion And Migration ◽  
Retraction Notice ◽  
And Migration

This article has been retracted.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

Kisspeptin-10 Inhibits Stromal-Derived Factor 1–Induced Invasion of Human Endometrial Cancer Cells

2014 ◽  
Vol 24 (2) ◽  
pp. 210-217 ◽  
Author(s):  
Elena Schmidt ◽  
Maike Haase ◽  
Elke Ziegler ◽  
Günter Emons ◽  
Carsten Gründker
Keyword(s):  
Endometrial Cancer ◽  
Basement Membrane ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Cell Invasion ◽  
Metastatic Cancer ◽  
Boyden Chamber ◽  
Cancer Cell Invasion ◽  
Endometrial Cancer Cell ◽  
Mg63 Cells

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.

Variances in the Expression Profile of the EMT-Related Genes in Endometrial Cancer Lines In Vitro Study

2021 ◽  
Vol 22 ◽  
Author(s):  
Robert Nowakowski ◽  
Beniamin Grabarek ◽  
Anna Burnat-Olech ◽  
Dariusz Boroń ◽  
Monika Paul-Samojedny
Keyword(s):  
Endometrial Cancer ◽  
Expression Pattern ◽  
Cell Lines ◽  
Cancer Cell ◽  
Cell Cultures ◽  
Expression Profile ◽  
Histological Grade ◽  
Cancer Cell Lines ◽  
Endometrial Cancer Cell

Background: This study aimed to evaluate the variances in the expression pattern of mRNAs and miRNAs related to the EMT in the Ishikawa (histological grade 1; G1), EC-1A (histological grade 2; G2), and KLE (histological grade 3; G3) cell cultures under cisplatin treatment. Methods: Endometrial cancer cell lines were exposed to 75.22 mg (an average concentration of the drug used in patients with endometrial cancer) for 12.24 and 48 hours compared to the untreated cells (control). The molecular analysis included extraction of total RNA, microarray analysis (mRNA and miRNA), RTqPCR, and the ELISA assay. Results: Out of 226 mRNAs associated with the EMT, the number of mRNAs differentially expressed in endometrial cancer cell cultures treated with cisplatin compared to a control culture was as follows: Ishikawa line - 87 mRNAs; EC-1A - 84 mRNAs; KLE - 71 mRNAs (p<0.05). The greatest changes in the Ishikawa line treated with the drug compared to the control were noticed for mRNA STAT1 TGFβ1, SMAD3, FOXO8, whereas in EC-1A, they were mRNA TGFβ1, BAMBI, SMAD4, and in KLE mRNA COL1A1, FOXO8, TGFβ1. The analysis also showed that miR-106a, miR-30d, miR-300 are common for all cell lines used in this experiment. Conclusion: Cisplatin changes the expression profile of genes associated with EMT in endometrial cancer cell lines. It seems that the expression pattern of TGFβ1 might be a promising, supplementary molecular marker of the effectiveness of cisplatin therapy. The analysis showed that miR-30d, miR-300, and miR-106a are involved in the regulation of the expression of EMT-related genes.

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