Transferred by exosomes-derived MiR-19b-3p targets PTEN to regulate esophageal cancer cell apoptosis, migration and invasion

Abstract The present study aims to investigate the relationship between miR-19b-3p and esophageal cancer (ESCA), and to detect the effects of miR-19b-3p transferred by exosomes on the phenotype of EC9706 cells. The expression of miR-19b-3p was detected by starBase analysis and real-time quantitative PCR (RT-qPCR). The target genes of miR-19b-3p were predicted by TargetScan and further verified by luciferase analysis. The mRNA and protein expression levels of PTEN and EMT-related genes were detected by RT-qPCR and Western blotting. The effects of miR-19b-3p transferred by exosomes and its target genes on the apoptosis, migration and invasion of EC9706 cells were studied by establishing a co-culture model of donor cells. The expression of miR-19b-3p in ESCA plasma, cells and exosomes was significantly up-regulated. miR-19b-3p transferred by exosomes could significantly reduce EC9706 cells apoptosis rate, promote cell migration and invasion, and could target the inhibition of PTEN expression. PTEN overexpression promoted apoptosis, inhibited cell migration and invasion, down-regulated the expression of MMP-2 and vimentin, and up-regulated E-cadherin expression; however, these effects could be partially reversed by miR-19b-3p. In summary, our results reveal that miR-19b-3p transferred by exosomes can target PTEN to regulate ESCA biological functions in the receptor EC9706 cells.

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Altered LKB1/CREB-regulated transcription co-activator (CRTC) signaling axis promotes esophageal cancer cell migration and invasion

Oncogene ◽

10.1038/onc.2011.247 ◽

2011 ◽

Vol 31 (4) ◽

pp. 469-479 ◽

Cited By ~ 58

Author(s):

Y Gu ◽

S Lin ◽

J-L Li ◽

H Nakagawa ◽

Z Chen ◽

...

Keyword(s):

Esophageal Cancer ◽

Cell Migration ◽

Cancer Cell ◽

Migration And Invasion ◽

Cancer Cell Migration ◽

Cell Migration And Invasion ◽

Signaling Axis ◽

Esophageal Cancer Cell

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Abstract 1059: Altered LKB1/CREB-regulated transcription co-activator (CRTC) signaling axis promotes esophageal cancer cell migration and invasion

10.1158/1538-7445.am2011-1059 ◽

2011 ◽

Author(s):

Yumei Gu ◽

Shuibin Lin ◽

Jian-Liang Li ◽

Hiroshi Nakagawa ◽

Zirong Chen ◽

...

Keyword(s):

Esophageal Cancer ◽

Cell Migration ◽

Cancer Cell ◽

Migration And Invasion ◽

Cancer Cell Migration ◽

Cell Migration And Invasion ◽

Signaling Axis ◽

Esophageal Cancer Cell

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HDL and sphingosine-1-phosphate activate stat3 in prostate cancer DU145 cells via ERK1/2 and S1P receptors, and promote cell migration and invasion

The Prostate ◽

10.1002/pros.21285 ◽

2010 ◽

Vol 71 (7) ◽

pp. 690-699 ◽

Cited By ~ 30

Author(s):

Yoshitaka Sekine ◽

Kazuhiro Suzuki ◽

Alan T. Remaley

Keyword(s):

Prostate Cancer ◽

Cell Migration ◽

Migration And Invasion ◽

Cell Migration And Invasion ◽

S1p Receptors ◽

Promote Cell Migration ◽

Sphingosine 1 Phosphate ◽

Du145 Cells

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T-cadherin deficiency promotes endometriosis progression through the PI3K/AKT/mTOR signaling pathway

10.21203/rs.3.rs-18041/v1 ◽

2020 ◽

Author(s):

yutao guan ◽

Fu-bin Zhang ◽

Yan-qing Huang ◽

Ling-ling Zhou ◽

Wei-feng Li ◽

...

Keyword(s):

Cell Migration ◽

Protein Expression ◽

Signaling Pathway ◽

Benign Disease ◽

Mtor Signaling ◽

Migration And Invasion ◽

Mtor Signaling Pathway ◽

Cell Migration And Invasion ◽

Female Patients ◽

Mrna And Protein Expression

Abstract Background: Endometriosis is a progressive and benign disease characterized by the presence of endometrial glands and stroma tissue outside of the uterine cavity. Though endometriosis is a benign disease, it has the characteristics of malignant tumour growth. Abnormal expression of T-cadherin is involved in the occurrence and progression of many tumours. We aimed to investigate whether T-cadherin promotes the migration and invasion of endometriosis cells through the PI3K/AKT/mTOR signaling pathway. Methods: Ectopic and eutopic endometrial samples from 62 female patients with endometriosis and endometrial samples from 51 female patients without endometriosis were collected. The immortalized endometrial stromal cell line hEM15A was cultured. Real-time RT-PCR, immunohistochemistry and Western blot were used to detect the expression of T-cadherin, phospho-PI3K/Akt/mTOR and matrix metalloproteinase 2 (MMP-2). Transfection technology was employed to upregulate T-cadherin expression. The migration and invasion abilities of hEM15A cells were measured by the transwell assay with uncoated or Matrigel-coated membranes. Results: The mRNA and protein expression of T-cadherin was significantly decresed in the ectopic tissues of the patients with endometriosis, while the mRNA and protein expression in the eutopic endometrial tissues of the same patients did not significantly differ from that in the patients without endometriosis. The migration and invasion ability and phospho-PI3K/Akt/mTOR and MMP-2 expression levels were decreased in hEM15A cells with high T-cadherin expression compared with the corresponding parameters in the normal control group. However, everolimus and BEZ235 inhibited cell migration and invasion in cells with low T-cadherin expression, and weakened overexpression of T‑cadherin significantly attenuated MMP-2 protein expression. Conclusion: Loss of T-cadherin promotes cell migration and invasion in endometriosis via the PI3K/AKT/mTOR signalling pathway.

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