scholarly journals Tumor-suppressor miRNA-27b-5p regulates the growth and metastatic behaviors of ovarian carcinoma cells by targeting CXCL1

2020 ◽  
Author(s):  
Chun Hua Liu ◽  
Xue Ning Jing ◽  
Xiao Lan Liu ◽  
Shan Yong Qin ◽  
Min Wei Liu ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Ovarian Carcinoma ◽  
Cancer Cells ◽  
Carcinoma Cells ◽  
Cell Counting ◽  
Luciferase Reporter ◽  
Ovarian Cancer Cells ◽  
Skov3 Cell ◽  
Ovarian Carcinoma Cells ◽  
The Impact

Abstract BackgroundMicroRNAs (miRNAs) play crucial functions in the progression of ovarian cancer. MicroRNA-27b-5p (miR-27b-5p) has been identified as a cancer-associated miRNA. Nevertheless, the expression profile of miR-27b-5p and its functions in ovarian cancer are unexplored.MethodsqRT-PCR and western blot analysis were used to detect the levels of miR-27b-5p and C-X-C motif chemokine ligand 1 (CXCL1). The impact of miR-27b-5p on ovarian cancer cells proliferation, migration and invasion in vitro were investigated using Cell Counting Kit-8 (CCK8), wound healing and Transwell, respectively. The expression of matrix metalloprotein-2/9 (MMP-2/9) were measured using immunofluorescence staining. Bioinformatics and luciferase reporter analysis were used to predict the target of miR-27b-5p. The growth of ovarian cancer cells in vivo was evaluated using transplanted tumor model.ResultsHere, we demonstrated that miR-27b-5p was downregulated in ovarian carcinoma cells and clinical specimens. Higher expression of miR-27b-5p was associated with an unfavorable overall survival in patients with ovarian cancer. Upregulation of miR-27b-5p decreased the viability, migration ability and invasion capacity of SKOV3 and OVCAR3 cell. MiR-27b-5p also inhibited the growth of SKOV3 cell in nude mice. Additionally, we verified that CXCL1 was a target of miR-27b-5p in ovarian carcinoma cells. Restoring the expression of CXCL1 abolished the inhibitory impacts of miR-27b-5p in ovarian cancer carcinoma cells.ConclusionThis research revealed that miR-27b-5p restrained the progression of ovarian carcinoma possibly via targeting CXCL1.

scholarly journals The interactions of human ovarian cancer cells and nanotextured surfaces: cell attachment, viability and apoptosis studies

RSC Advances ◽  
2019 ◽  
Vol 9 (45) ◽  
pp. 25957-25966
Author(s):  
Gökçen Yaşayan ◽  
Oya Orun ◽  
Pınar Mega Tiber ◽  
Veronika Rožman ◽  
Sevgi Koçyiğit Sevinç
Keyword(s):  
Ovarian Cancer ◽  
Ovarian Carcinoma ◽  
Cancer Cells ◽  
Cell Attachment ◽  
Carcinoma Cells ◽  
Ovarian Cancer Cells ◽  
Human Ovarian Cancer ◽  
Ovarian Carcinoma Cells ◽  
Human Ovarian Carcinoma ◽  
Human Ovarian Carcinoma Cells

Fabrication and characterisation studies of nanotextured polycaprolactone surfaces, and an investigation of their influence on human ovarian carcinoma cells.

The Impact of Paclitaxel-Containing Nanoliposomes on the Proliferation of and Invasion by Ovarian Cancer Cells

2020 ◽  
Vol 12 (3) ◽  
pp. 361-367
Author(s):  
Xiaoping Chen ◽  
Xinping Ren ◽  
Jinling Xue ◽  
Ling Xi
Keyword(s):  
Ovarian Cancer ◽  
Ovarian Carcinoma ◽  
Carcinoma Cells ◽  
Ovarian Cancer Cells ◽  
Qrt Pcr ◽  
Ovarian Carcinoma Cells ◽  
Effective Inhibition ◽  
Matrix Metallopeptidase ◽  
The Impact ◽  
Invasion Assays

Our goal was to explore the impact of paclitaxel-containing nanoliposomes (PTXN) on the proliferation of and invasion by ovarian carcinoma cells. An MTT assay was used to examine growth of SKOV3 and HO8910 ovarian carcinoma cells in the presence of paclitaxel (TAX) alone or PTXN. Transwell invasion assays were performed; Western blot and qRT-PCR were used to examine expression of matrix metallopeptidase (MMP)-9. PTXN administered at concentrations from 0.625–10 μg/mL was more effective at inhibiting the proliferation of SKOV3 and HO8910 cells than was TAX alone (P < 0.05). Administration of PTXN to these cells reduced their capacity for invasion, and expression of MMP-9 mRNA and protein over that achieved by administration of TAX alone (P < 0.05). PTXN promotes more effective inhibition of invasion of ovarian carcinoma cells than does TAX alone.

Platinum(ii) complexes showing high cytotoxicity toward A2780 ovarian carcinoma cells

2019 ◽  
Vol 48 (34) ◽  
pp. 13081-13093 ◽  
Author(s):  
Katarzyna Choroba ◽  
Barbara Machura ◽  
Luis R. Raposo ◽  
Jan G. Małecki ◽  
Slawomir Kula ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Ovarian Carcinoma ◽  
Cytotoxic Activity ◽  
Cancer Cells ◽  
Carcinoma Cells ◽  
Ovarian Cancer Cells ◽  
Ovarian Carcinoma Cells ◽  
High Cytotoxicity ◽  
High Cytotoxic Activity

2,6-Bis(thiazol-2-yl)pyridines functionalized with 9-anthryl (L1), 9-phenanthryl (L2), and 1-pyrenyl (L3) groups were used for the preparation of [Pt(Ln)Cl]CF3SO3 (1–3) with high cytotoxic activity against ovarian cancer cells.

Carboplatin-induced Senescence in Ovarian Cancer Cells Is Reversed Through EGFR and NF-κB Signaling

2021 ◽  
Author(s):  
Yue Li ◽  
Mingxu Fu ◽  
Ling Guo ◽  
Xiaoxiao Sun ◽  
Yuhang Chen ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Western Blot ◽  
Cancer Cells ◽  
Blot Analysis ◽  
Western Blot Analysis ◽  
Cell Counting ◽  
Blue Staining ◽  
Ovarian Cancer Cells ◽  
Positive Staining ◽  
The Impact

Abstract Background: Metastases and recurrence of ovarian cancer after surgery and chemotherapy account for most cancer-related deaths, yet the mechanism underlying metastases and recurrence remains poorly understood. Recent evidence demonstrates that although long-lasting cells were considered tumor suppressors, senescent cancer cells, can induce the metastases and recurrence. In this study, we focused on the fate of ovarian cancer cells treated with carboplatin and explored the mechanism underlying ovarian cancer cell recovery from chemotherapy-induced senescence. Methods: SÁ-β-galactosidase staining was used to detect the impact of carboplatin on senescence of ovarian cancer cells. Cell proliferation was determined using direct cell counting, clone formation assay and 3D tumor spheroid formation assay. Lentivirus-mediated transduction was used to silence or upregulate EGFR expression. Quantitative real-time PCR and western blot analysis validated the efficacy of the knockdown or overexpression effect. Immunofluorescence staining and western blot analysis were used to examined the expression of EGFR and NF-KB. Cell death was determined using trypan blue staining assay. Results: Ovarian cancer cells treated by carboplatin exhibit a senescence-like phenotype indicated by SA-β-galactosidase positive staining. Importantly, carboplatin-induced senescence-like phenotype is reversible. In ovarian cancer cells, EGFR positively regulated cells proliferation, decreased carboplatin-induced senescence and upregulated the NF-κB1 protein level. EGFR/NF-κB1 upregulation promoted the recovery of ovarian cancer cells from senescence and chemoresistance to carboplatin. Conclusions: Ovarian cancer cells treated with carboplatin displayed a reversible senescence-like phenotype that could be combined with EGFR or NF-κB1 inhibitors to improve treatment effects.

scholarly journals miR-552 promotes ovarian cancer progression by regulating PTEN pathway

2019 ◽  
Vol 12 (1) ◽  
Author(s):  
Wenman Zhao ◽  
Tao Han ◽  
Bao Li ◽  
Qianyun Ma ◽  
Pinghua Yang ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Cancer Cells ◽  
Cancer Progression ◽  
Malignant Tumors ◽  
Luciferase Reporter ◽  
Ovarian Cancer Cells ◽  
Cancer Proliferation ◽  
Proliferation And Metastasis ◽  
The Impact

Abstract Background Increasing researches have demonstrated the critical functions of MicroRNAs (miRNAs) in the progression of malignant tumors, including ovarian cancer. It was reported that miR-552 was an important oncogene in both breast cancer and colorectal cancer. However, the role of miR-552 in ovarian cancer (OC) remains to be elucidated. Methods RT-PCR and western blot analysis were used to detect the expression of miR-552 and PTEN. The impact of miR-552 on ovarian cancer proliferation and metastasis was investigated in vitro. The prognostic value of miR-552 was evaluated using the online bioinformatics tool Kaplan-Meier plotter. Results In the present study, we for first found that miR-552 was upregulated in ovarian cancer, especially in metastatic and recurrence ovarian cancer. Forced miR-552 expression promotes the growth and metastasis of ovarian cancer cells. Consistently, miR-552 interference inhibits the proliferation and metastasis of ovarian cancer cells. Mechanically, bioinformatics and luciferase reporter analysis identified Phosphatase and tension homolog (PTEN) as a direct target of miR-552. miR-552 downregulated the PTEN mRNA and protein expression in ovarian cancer cells. Furthermore, the PTEN siRNA abolishes the discrepancy of growth and metastasis capacity between miR-552 mimic ovarian cells and control cells. More importantly, upregulation of miR-552 predicts the poor prognosis of ovarian cancer patients. Conclusion Our findings revealed that miR-552 could promote ovarian cancer cells progression by targeting PTEN signaling and might therefore be useful to predict patient prognosis.

scholarly journals CircASH2L Promotes Ovarian Cancer Tumorigenesis, Angiogenesis, and Lymphangiogenesis by Regulating the miR-665/VEGFA Axis as a Competing Endogenous RNA

2020 ◽  
Vol 8 ◽  
Author(s):  
Jinxin Chen ◽  
Xiaocen Li ◽  
Lu Yang ◽  
Mengmeng Li ◽  
Ye Zhang ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Cancer Cells ◽  
Molecular Mechanisms ◽  
Critical Role ◽  
Gynecologic Cancer ◽  
Luciferase Reporter ◽  
Circular Rnas ◽  
Ovarian Cancer Cells ◽  
Western Blots ◽  
The Impact

Ovarian cancer is the leading cause of gynecologic cancer-related deaths. Emerging research has revealed a close relationship between circular RNAs (circRNAs) and ovarian cancer development, metastasis, and prognosis. The objective of our research was to further explore the relationship between circASH2L and ovarian cancer. Quantitative real-time polymerase chain reaction was used to detect the differential expression of circRNAs between normal ovaries and ovarian cancer tissues. The impact of circASH2L on the proliferation, invasion, and tumorigenicity of ovarian cancer cells was evaluated using gain- and loss-of-function experiments. The molecular mechanisms of circASH2L function were investigated using bioinformatics analysis, RNA fluorescence in situ hybridization, western blots, and dual-luciferase reporter assays. The results showed that circASH2L was remarkably upregulated in ovarian cancer. The invasion and growth of ovarian cancer cells were suppressed by circASH2L knockdown in vitro, and downregulation of circASH2L restrained both angiogenesis and lymphangiogenesis of tumor xenografts in vivo. Furthermore, circASH2L was mostly distributed in the cytoplasm, where it competes with vascular endothelial growth factor A (VEGFA) for binding to miR-665. These findings indicate that circASH2L has an oncogenic function in ovarian cancer. In conclusion, circASH2L plays a critical role in regulating ovarian cancer cell tumorigenesis, angiogenesis, and lymphangiogenesis through the miR-665/VEGFA axis and, therefore, is a possible candidate target for ovarian cancer treatment.

scholarly journals Inhibition of calcium-independent phospholipase A2 suppresses proliferation and tumorigenicity of ovarian carcinoma cells

2007 ◽  
Vol 406 (3) ◽  
pp. 427-436 ◽  
Author(s):  
Yuanda Song ◽  
Palmer Wilkins ◽  
Wenhui Hu ◽  
Karnam S. Murthy ◽  
Jing Chen ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Ovarian Cancer ◽  
Growth Factors ◽  
Growth Factor ◽  
Ovarian Carcinoma ◽  
Carcinoma Cells ◽  
Ovarian Cancer Cells ◽  
Ovarian Carcinoma Cells ◽  
Phase Arrest ◽  
M Phase

PLA2 (phospholipase A2) enzymes play critical roles in membrane phospholipid homoeostasis and in generation of lysophospholipid growth factors. In the present study, we show that the activity of the cytosolic iPLA2 (calcium-independent PLA2), but not that of the calcium-dependent cPLA2 (cytosolic PLA2), is required for growth-factor-independent, autonomous replication of ovarian carcinoma cells. Blocking iPLA2 activity with the pharmacological inhibitor BEL (bromoenol lactone) induces cell cycle arrest in S- and G2/M-phases independently of the status of the p53 tumour suppressor. Inhibition of iPLA2 activity also leads to modest increases in apoptosis of ovarian cancer cells. The S- and G2/M-phase accumulation is accompanied by increased levels of the cell cycle regulators cyclins B and E. Interestingly, the S-phase arrest is released by supplementing the growth factors LPA (lysophosphatidic acid) or EGF (epidermal growth factor). However, inhibition of iPLA2 activity with BEL remains effective in repressing growth-factor- or serum-stimulated proliferation of ovarian cancer cells through G2/M-phase arrest. Down-regulation of iPLA2β expression with lentivirus-mediated RNA interference inhibited cell proliferation in culture and tumorigenicity of ovarian cancer cell lines in nude mice. These results indicate an essential role for iPLA2 in cell cycle progression and tumorigenesis of ovarian carcinoma cells.

scholarly journals Exosomal microRNA-205 is involved in proliferation, migration, invasion, and apoptosis of ovarian cancer cells via regulating VEGFA

2019 ◽  
Vol 19 (1) ◽  
Author(s):  
Lijun Wang ◽  
Fei Zhao ◽  
Zhongqing Xiao ◽  
Liang Yao
Keyword(s):  
Ovarian Cancer ◽  
Cancer Cells ◽  
Diagnostic Value ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Ovarian Cancer Cells ◽  
Mesenchymal Transition ◽  
Skov3 Cells ◽  
Gene Assay ◽  
The Impact

Abstract Background Recently, the impact of microRNAs (miRNAs) and exosome on ovarian cancer has been assessed in many studies. We aim to explore the mechanism of exosomes transferring miR-205 in ovarian cancer, and confirm its diagnostic value in ovarian cancer. Methods The expression of miR-205 of ovarian cancer patients and healthy people was detected by RT-qPCR, and the diagnostic value of miR-205 was evaluated. The exosomes derived from SKOV3 cells were identified. Ovarian cancer SKOV3 donor cells and receptor cells were used to measure the proliferation, migration, invasion, apoptosis and cell cycle by a series of experiments. The binding site between miR-205 and vascular endothelial growth factor A (VEGFA) was evaluated by bioinformatics tool and dual-luciferase reporter gene assay. Results MiR-205 was up-regulated in ovarian cancer, and up-regulated miR-205 could enhance the risk of ovarian cancer and was one of its risk factors. After SKOV3 cells-derived exosomes were transiently introduced with miR-205 mimics, the cell proliferation, migration and invasion in ovarian cancer were elevated, the apoptosis of ovarian cancer cells was attenuated, and the epithelial–mesenchymal transition (EMT) protein E-cadherin was down-regulated, while Vimentin was elevated. VEGFA was identified to be a target gene of miR-205. Conclusion This study suggests that exosomes from donor ovarian cancer cell SKOV3 shuttled miR-205 could participate in the regulation of the proliferation, migration, invasion, apoptosis as well as EMT progression of receptor SKOV3 cells by targeting VEGFA.

scholarly journals Tumor-suppressor miRNA-27b-5p regulates the growth and metastatic behaviors of ovarian carcinoma cells by targeting CXCL1

2020 ◽  
Author(s):  
Shan Yong Qin ◽  
Min Wei Liu
Keyword(s):  
Ovarian Cancer ◽  
Ovarian Carcinoma ◽  
Ovarian Cancer Patient ◽  
Carcinoma Cell ◽  
Carcinoma Cells ◽  
Skov3 Cell ◽  
Migration Ability ◽  
Ovarian Carcinoma Cells ◽  
A2780 Cell ◽  
Chemokine Ligand

Abstract MicroRNAs (miRNAs) play crucial functions in the progression of ovarian cancer. MiR-27b has been identified as cancer-associated miRNA. Nevertheless, the expression profile of microRNA-27b-5p (miR-27b-5p) and its functions in ovarian cancer are unexplored. Here, we demonstrated that miR-27b-5p was downregulated in ovarian carcinoma cells and clinical specimens. Higher expression of miR-27b-5p was allied to an unfavorable overall survival in ovarian cancer patient. Upregulation of miR-27b-5p decreased the viability, migration ability and invasion capacity of SKOV3 and A2780 cell. MiR-27b-5p also inhibited the growth of SKOV3 cell in nude mice. Additionally, we verified that C-X-C motif chemokine ligand 1 (CXCL1) was a target of miR-27b-5p in ovarian carcinoma cell. Restoring the expression of CXCL1 abolished the inhibitory impacts of miR-27b-5p in ovarian cancer carcinoma cell. This research revealed that miR-27b-5p restrained the progression of ovarian carcinoma possibly via targeting CXCL1.

scholarly journals Propofol suppresses cell viability, cell cycle progression and motility and induces cell apoptosis of ovarian cancer cells through suppressing MEK/ERK signaling via targeting circVPS13C/miR-145 axis

2021 ◽  
Vol 14 (1) ◽  
Author(s):  
Huan Lu ◽  
Guanlin Zheng ◽  
Xiang Gao ◽  
Chanjuan Chen ◽  
Min Zhou ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Ovarian Cancer ◽  
Cancer Cells ◽  
Rna Binding ◽  
Erk Signaling ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Ovarian Cancer Cells ◽  
Dependent Manner ◽  
Vacuolar Protein

Abstract Background Propofol is a kind of common intravenous anaesthetic agent that plays an anti-tumor role in a variety of cancers, including ovarian cancer. However, the working mechanism of Propofol in ovarian cancer needs further exploration. Methods The viability and metastasis of ovarian cancer cells were assessed by 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay and transwell assays. Flow cytometry was used to evaluate the cell cycle and apoptosis. Quantitative real-time polymerase chain reaction (qRT-PCR) was used to examine the abundance of circular RNA vacuolar protein sorting 13 homolog C (circVPS13C) and microRNA-145 (miR-145). The target relationship between miR-145 and circVPS13C was predicted by circinteractome database and verified by dual-luciferase reporter assay, RNA-binding protein immunoprecipitation (RIP) assay and RNA-pull down assay. Western blot assay was used to detect the levels of phosphorylated extracellular regulated MAP kinase (p-ERK), ERK, p-MAP kinse-ERK kinase (p-MEK) and MEK, in ovarian cancer cells. Results Propofol treatment suppressed the viability, cell cycle and motility and elevated the apoptosis rate of ovarian cancer cells. Propofol up-regulated miR-145 in a dose-dependent manner. Propofol exerted an anti-tumor role partly through up-regulating miR-145. MiR-145 was a direct target of circVPS13C. Propofol suppressed the progression of ovarian cancer through up-regulating miR-145 via suppressing circVPS13C. Propofol functioned through circVPS13C/miR-145/MEK/ERK signaling in ovarian cancer cells. Conclusion Propofol suppressed the proliferation, cell cycle, migration and invasion and induced the apoptosis of ovarian cancer cells through circVPS13C/miR-145/MEK/ERK signaling in vitro.

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