scholarly journals circ-CSPP1 promotes proliferation, invasion and migration of ovarian cancer cells by acting as a miR-1236-3p sponge

2019 ◽  
Vol 114 ◽  
pp. 108832 ◽  
Author(s):  
Qian-hui Li ◽  
Yao Liu ◽  
Shuo Chen ◽  
Zhi-hong Zong ◽  
Yu-ping Du ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Cancer Cells ◽  
Ovarian Cancer Cells ◽  
Invasion And Migration ◽  
And Migration

scholarly journals Long non-coding RNA XIST regulates ovarian cancer progression via modulating miR-335/BCL2L2 axis

2021 ◽  
Vol 19 (1) ◽  
Author(s):  
Qingjuan Meng ◽  
Ningning Wang ◽  
Guanglan Duan
Keyword(s):  
Ovarian Cancer ◽  
Cancer Cells ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Ovarian Cancer Cells ◽  
Human Ovarian Cancer ◽  
Invasion And Migration ◽  
Non Coding Rna ◽  
And Migration ◽  
Long Non Coding Rna

Abstract Background X inactivation-specific transcript (XIST) is the long non-coding RNA (lncRNA) related to cancer, which is involved in the development and progression of various types of tumor. However, up to now, the exact role and molecular mechanism of XIST in the progression of ovarian cancer are not clear. We studied the function of XIST in ovarian cancer cells and clinical tumor specimens. Methods RT-qPCR was performed to detect the expression levels of miR-335 and BCL2L2 in ovarian cancer cells and tissues. MTT and transwell assays were carried out to detect cell proliferation, migration, and invasion abilities. Western blot was performed to analyze the expression level of BCL2L2. The interaction between miR-335 and XIST/BCL2L2 was confirmed using a luciferase reporter assay. Results The inhibition of XIST can inhibit the proliferation invasion and migration of human ovarian cancer cells. In addition, the miR-335/BCL2L2 axis was involved in the functions of XIST in ovarian cancer cells. These results suggested that XIST could regulate tumor proliferation and invasion and migration via modulating miR-335/BCL2L2. Conclusion XIST might be a carcinogenic lncRNA in ovarian cancer by regulating miR-335, and it can serve as a therapeutic target in human ovarian cancer.

LncRNA MEG3 impacts proliferation, invasion, and migration of ovarian cancer cells through regulating PTEN

2018 ◽  
Vol 67 (11-12) ◽  
pp. 927-936 ◽  
Author(s):  
Juelan Wang ◽  
Wenqian Xu ◽  
Yangke He ◽  
Qi Xia ◽  
Siwei Liu
Keyword(s):  
Ovarian Cancer ◽  
Cancer Cells ◽  
Ovarian Cancer Cells ◽  
Invasion And Migration ◽  
And Migration

scholarly journals High LIN28A Expressing Ovarian Cancer Cells Secrete Exosomes That Induce Invasion and Migration in HEK293 Cells

2015 ◽  
Vol 2015 ◽  
pp. 1-13 ◽  
Author(s):  
Vanessa A. Enriquez ◽  
Ellane R. Cleys ◽  
Juliano C. Da Silveira ◽  
Monique A. Spillman ◽  
Quinton A. Winger ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Epithelial Ovarian Cancer ◽  
Cancer Cells ◽  
Rna Binding ◽  
Tumor Development ◽  
Hek293 Cells ◽  
Ovarian Cancer Cells ◽  
Mesenchymal Transition ◽  
Invasion And Migration ◽  
And Migration

Epithelial ovarian cancer is the most aggressive and deadly form of ovarian cancer and is the most lethal gynecological malignancy worldwide; therefore, efforts to elucidate the molecular factors that lead to epithelial ovarian cancer are essential to better understand this disease. Recent studies reveal that tumor cells release cell-secreted vesicles called exosomes and these exosomes can transfer RNAs and miRNAs to distant sites, leading to cell transformation and tumor development. The RNA-binding protein LIN28 is a known marker of stem cells and when expressed in cancer, it is associated with poor tumor outcome. We hypothesized that high LIN28 expressing ovarian cancer cells secrete exosomes that can be taken up by nontumor cells and cause changes in gene expression and cell behavior associated with tumor development. IGROV1 cells were found to contain high LIN28A and secrete exosomes that were taken up by HEK293 cells. Moreover, exposure to these IGROV1 secreted exosomes led to significant increases in genes involved in Epithelial-to-Mesenchymal Transition (EMT), induced HEK293 cell invasion and migration. These changes were not observed with exosomes secreted by OV420 cells, which contain no detectable amounts of LIN28A or LIN28B. No evidence was found of LIN28A transfer from IGROV1 exosomes to HEK293 cells.

scholarly journals SFRP2 Promotes Peritoneal Metastasis of Ovarian Cancer within Phosphorylation of GSK3β

2021 ◽  
Author(s):  
Tengfei Zhang ◽  
Shimin Chen Qin ◽  
Jianrong Yuan ◽  
Jianlong Zhao ◽  
Yutong Wang ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Cancer Cells ◽  
Peritoneal Metastasis ◽  
Biological Effects ◽  
High Expression ◽  
Ovarian Cancer Cells ◽  
Sequencing Data ◽  
Data Set ◽  
Invasion And Migration ◽  
And Migration

Abstract BackgroundThe aim was to study further the molecular mechanism of ovarian cancer peritoneal metastasis and the corresponding prognostic markers.MaterialsWe analysed the sequencing data of 10 pairs of primary ovarian cancer and peritoneal metastasis from GSE98281 to determine SFRP2 through GO, KEGG and GSEA analysis. Western blot, invasion and migration experiments were used to detect the biological effects of SFRP2 on ovarian cancer cells. Immunohistochemistry was used to detect ovarian cancer in tissue samples from a TCGA-Ovarian Cancer cohort, and the survival analysis of SFRP2 was then performed.ResultsSFRP2 affected the phosphorylation level of GSK3β and upregulated the expression level of β-catenin. The high expression of SFRP2 in ovarian cancer cells improves cell invasion and migration capabilities. In histology studies, high expression of SFRP2 has increased the positive expression of β-catenin in the nucleus, and patients with high expression of SFRP2 had a worse prognosis. Similar results also appeared in ovarian cancer cases with high expression of SFRP2 mRNA in the TCGA data set.ConclusionSFRP2 activates the β-Catenin/Wnt signalling pathway through phosphorylation of GSK3β, which promotes the metastasis of ovarian cancer that leads to poor prognosis.

scholarly journals microRNA-4488 in extracellular vesicles derived from marrow mesenchymal stem cells suppresses ABHD8 to inhibit ovarian cancer progression

2020 ◽  
Author(s):  
Lei Chang ◽  
Junying Zhou ◽  
Wanjia Tian ◽  
Mengyu Chen ◽  
Ruixia Guo ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Cell Proliferation ◽  
Cancer Cells ◽  
Cancer Progression ◽  
Luciferase Reporter ◽  
Ovarian Cancer Cells ◽  
Invasion And Migration ◽  
And Migration

Abstract Background Extracellular vesicle (EV) that delivered microRNAs (miRNAs) have been found as the important biomarkers participating in the pathological mechanism of ovarian cancer. Consequently, this study sought to examine the underlying mechanism of mesenchymal stem cell (MSC)-derived EVs containing miR-4488 in ovarian cancer. Methods The normal ovarian tissues and ovarian cancer tissues were extracted, and the information of MSC-EV miRNA was obtained by Bioinformatics analysis. RT-qPCR and western blot analysis were applied to detect miR-4488 and α/β-hydrolase domain-containing (ABHD)8 expression followed by determination of relationship between miR-4488 and ABHD8 by dual-luciferase reporter assay. After transfection with different plasmids and treatment with DMSO or GW4869 (inhibitor of EV), the regulatory roles of MSC-EV-miR-4488 in invasion, proliferation, apoptosis, and migration of cancer cells were explored. Besides, xenograft tumor in nude mice was conducted to explore the role of miR-4488 and ABHD8 in ovarian cancer in vivo. Results miR-4488 was poorly expressed and ABHD8 was highly expressed in ovarian cancer cells and tissues. ABHD8 was a target gene of miR-4488 while the knockdown of ABHD8 resulted in the suppression of proliferation, invasion, and migration while promoting the apoptosis of cancer cells. Functionally, MSC-EV-derived miR-4488 inhibited the expression of ABHD8. Additionally, miR-4488 over-expressed in MSC-EVs inhibited the cell proliferation, invasion, and migration through down-regulation of ABHD8 expression. At last, these in vitro findings were also confirmed in vivo. Conclusion To summarize, miR-4488 overexpressed in MSC-EVs suppressed ABHD8 expression to inhibit the cancer cell proliferation, invasion, and migration, thus suppressing ovarian cancer.

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