RETRACTED ARTICLE: LncRNA CTBP1-AS2 sponges miR-216a to upregulate PTEN and suppress endometrial cancer cell invasion and migration

Wang, Qinganzi; Yang, Yongxiu; Liang, Xiaolei

doi:10.1186/s13048-020-00639-2

Cited by 17 publications

(11 citation statements)

References 17 publications

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“…Another critical conclusion was that exosomal miR‐139‐5p could downregulate PTEN and trigger the ERK/MMP‐2 pathway. It was stated that PTEN was strongly connected to various tumors, including breast, endometrial and esophageal squamous cell carcinomas 31–33 . More specifically, PTEN was also found to play a part in trophoblast cell proliferation and PE development regulated by long noncoding RNA T cell leukemia/lymphoma 6 34 .…”

Section: Discussionmentioning

confidence: 99%

“…It was stated that PTEN was strongly connected to various tumors, including breast, endometrial and esophageal squamous cell carcinomas. [31][32][33] More specifically, PTEN was also found to play a part in trophoblast cell proliferation and PE development regulated by long noncoding RNA T cell leukemia/lymphoma 6. 34 Moreover, strengthened PTEN in HTR-8/SVneo cells displayed partial degeneration of the improved cell infiltration prompted by miR-21.…”

Section: Ameliorative Effect Of Exosomes On Pe Ratsmentioning

confidence: 99%

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Exosomal microRNA‐139‐5p from mesenchymal stem cells accelerates trophoblast cell invasion and migration by motivation of the ERK/MMP‐2 pathway via downregulation of protein tyrosine phosphatase

Liu

Wang²,

Zhang³

et al. 2020

J of Obstet and Gynaecol

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Aim: Exosomes present essential roles for intercellular interaction via extracellular pathways during systemic dysfunctions, including preeclampsia (PE). Here, we assessed the specific mechanism of mesenchymal stem cells (MSC)-originated exosomes in PE. Methods: The effects of exosomes on trophoblasts were studied by EdU, wound healing, Transwell and TUNEL assays. By microarray analysis, we found that exosomes enhanced the microRNA-139-5p (miR-139-5p) in trophoblasts, and confirmed the target gene of miR-139-5p by bioinformatics prediction and dualluciferase reporter gene assay. At the same time, ERK/MMP-2 pathway-related biomolecules were assessed through Western blot analysis. The pathway inhibitor was used for rescue experiments. Finally, the effect of exosomes on the pathology of PE rats was verified by in vivo experiments. Results: The exosomes originated from hucMSC fostered the trophoblast cell migration, invasion and proliferation and obstructed apoptosis. Moreover, miR-139-5p could be transmitted to trophoblasts through hucMSC-secreted exosomes. miR-139-5p targeted protein tyrosine phosphatase (PTEN), which regulated the ERK/MMP-2 pathway. Inhibition of the ERK/MMP-2 pathway significantly reduced the promoting effect of exosomes on trophoblasts. Treatment with exosomes significantly lowered blood pressure values and reduced 24-h proteinuria in PE rats. Conclusion: hucMSC-originated exosomes overexpressing miR-139-5p activated the ERK/MMP-2 pathway via PTEN downregulation, thus accelerating trophoblast cell invasion and migration, and blocking apoptosis. These results demonstrated that hucMSC-derived exosomes overexpressing miR-139-5p might be an innovative direction for therapeutic approaches against PE.

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Section: Discussionmentioning

confidence: 99%

Section: Ameliorative Effect Of Exosomes On Pe Ratsmentioning

confidence: 99%

Exosomal microRNA‐139‐5p from mesenchymal stem cells accelerates trophoblast cell invasion and migration by motivation of the ERK/MMP‐2 pathway via downregulation of protein tyrosine phosphatase

Liu

Wang²,

Zhang³

et al. 2020

J of Obstet and Gynaecol

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“…Although a tumor-suppressive role for miR-216a has been reported ( Zhang et al, 2017 ), this miRNA was identified as an oncogenic miRNA in many cancers, including EC ( Wang Q.A. et al, 2020 ), ovarian cancer ( Liu et al, 2017 ), hepatocellular carcinoma ( Xia et al, 2013 ), and renal cell carcinoma ( Chen et al, 2018 ).…”

Section: Discussionmentioning

confidence: 99%

“…et al, 2020 ), ovarian cancer ( Liu et al, 2017 ), hepatocellular carcinoma ( Xia et al, 2013 ), and renal cell carcinoma ( Chen et al, 2018 ). The direct target genes of miR-216a include PTEN in EC ( Wang Q.A. et al, 2020 ), and PTEN and SMAD7 in hepatocellular carcinoma ( Xia et al, 2013 ).…”

Section: Discussionmentioning

confidence: 99%

PD-L1 Is a Tumor Suppressor in Aggressive Endometrial Cancer Cells and Its Expression Is Regulated by miR-216a and lncRNA MEG3

Dong

Xiong

et al. 2020

Front. Cell Dev. Biol.

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BackgroundPoorly differentiated endometrioid adenocarcinoma and serous adenocarcinoma represent an aggressive subtype of endometrial cancer (EC). Programmed death-ligand-1 (PD-L1) was known to exhibit a tumor cell-intrinsic function in mediating immune-independent tumor progression. However, the functional relevance of tumor cell-intrinsic PD-L1 expression in aggressive EC cells and the mechanisms regulating its expression remain unknown.MethodsPD-L1 expression in 65 EC tissues and 18 normal endometrium samples was analyzed using immunohistochemical staining. The effects of PD-L1 on aggressive EC cell growth, migration and invasion were investigated by cell functional assays. Luciferase reporter assays were used to reveal the microRNA-216a (miR-216a)-dependent mechanism modulating the expression of PD-L1.ResultsPositive PD-L1 expression was identified in 84% of benign cases but only in 12% of the EC samples, and the staining levels of PD-L1 in EC tissues were significantly lower than those in the normal tissues. Higher PD-L1 expression predicts favorable survival in EC. Ectopic expression of PD-L1 in aggressive EC cells results in decreased cell proliferation and the loss of mesenchymal phenotypes. Mechanistically, PD-L1 exerts the anti-tumor effects by downregulating MCL-1 expression. We found that PD-L1 levels in aggressive EC cells are regulated by miR-216a, which directly targets PD-L1. We further identified a mechanism whereby the long non-coding RNA MEG3 represses the expression of miR-216a, thereby leading to increased PD-L1 expression and significant inhibition of cell migration and invasion.ConclusionThese results reveal an unappreciated tumor cell-intrinsic role for PD-L1 as a tumor suppressor in aggressive EC cells, and identify MEG3 and miR-216a as upstream regulators of PD-L1.

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“…The Editors-in-Chief has retracted this article [ 1 ] due to lack of evidence that the study has received ethics approval. After publication it has come to the Editor’s attention that in the body of the article the authors state that their study was approved by the Ethics Committee at the First Hospital of Lanzhou University.…”

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confidence: 99%

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

2020

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

Cited by 17 publications

References 17 publications

Exosomal microRNA‐139‐5p from mesenchymal stem cells accelerates trophoblast cell invasion and migration by motivation of the ERK/MMP‐2 pathway via downregulation of protein tyrosine phosphatase

Exosomal microRNA‐139‐5p from mesenchymal stem cells accelerates trophoblast cell invasion and migration by motivation of the ERK/MMP‐2 pathway via downregulation of protein tyrosine phosphatase

PD-L1 Is a Tumor Suppressor in Aggressive Endometrial Cancer Cells and Its Expression Is Regulated by miR-216a and lncRNA MEG3

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

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