Radix Tetrastigma Hemsleyani Flavone Inhibits the Occurrence and Development of Ovarian Cancer Cells by Regulating miRNA-4458 Expression

2021 ◽  
Vol 11 (3) ◽  
pp. 478-484
Author(s):  
Ping Liu ◽  
Yanjuan Guo ◽  
Yanfang He ◽  
Yajuan Tang
Keyword(s):  
Ovarian Cancer ◽  
Cell Proliferation ◽  
Protein Expression ◽  
Cyclin D1 ◽  
Cancer Cells ◽  
Diagnostic Methods ◽  
Migration And Invasion ◽  
Skov3 Cell ◽  
Advanced Stage ◽  
P21 Protein

Ovarian cancer (OC) has been identified to have the highest mortality rate among gynecological tumors. Most patients are diagnosed at an advanced stage because of its asymptomatic nature and a lack of effective early diagnostic methods. Advanced-stage cancer cells are prone to metastasis which reduces the efficacy of standard therapies. Thus, we evaluated the effect of different concentrations of radix tetrastigma hemsleyani flavone (RTHF) on SKOV3 OC cells. Our findings indicated a significant inhibition in cell proliferation, migration, and invasion. RTHF treatment resulted in a significant increase in p21 protein expression, whereas the expression of cyclin D1, MMP-2, and MMP-9 has reportedly decreased. In addition, the expression of miRNA-4458 expression increased significantly in a dose-dependent manner. Co-transfection of miRNA-4458 mimics into SKOV3 cells revealed that overexpressed miRNA-4458 can increase SKOV3 cell proliferation and p21 protein expression. Reduced cell migration and invasion were also observed along with decreased expression of cyclin D1, MMP-2, and MMP-9. Furthermore, inhibition of miRNA-4458 expression reversed the RTHF effect on SKOV3 cell proliferation, migration, invasion, and cyclin D1, MMP-2, and MMP-9 expression. These results indicate that RTHF reduces the proliferation, migration, and invasion of OC cells, and the underlying mechanism is associated with the upregulation of miRNA-4458 expression. These findings provide a new treatment strategy for advanced OC.

Tunneling nanotubes and intercellular communication: Differences between platinum-resistant and platinum-sensitive ovarian cancer.

2013 ◽  
Vol 31 (15_suppl) ◽  
pp. e22007-e22007
Author(s):  
Elizabeth Louise Dickson ◽  
Venugopal Thayanithy ◽  
Rachel Isaksson Vogel ◽  
Peter Argenta ◽  
Melissa Ann Geller ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Cell Proliferation ◽  
Cancer Cells ◽  
Cell Lines ◽  
Ovarian Cancer Cells ◽  
Platinum Resistance ◽  
Skov3 Cell ◽  
Continuous Exposure ◽  
Tunneling Nanotubes ◽  
Platinum Sensitive

e22007 Background: Preliminary evidence suggests that cell-to-cell communication may be responsible for the development of chemotherapy resistance in ovarian cancer. We propose tunneling nanotubes (TnTs) – long, thin actin-based cell extensions – as novel candidates to explain direct communication between treatment-refractory malignant ovarian cells. The purpose of this study was to investigate TnT formation between ovarian cancer cells in vitro. Methods: Using platinum-sensitive (A2780) and resistant (C200 and SKOV3, as well as ES2) ovarian cancer cell lines, we tested various conditions to assess factors affecting TnT formation. Scratch assays were utilized as a 2-dimensional simulation of ovarian cancer invasion. To assess TnTs as a conduit for transmission of therapeutic drugs between connected cells, we used doxorubicin, which auto-fluoresces in cell culture. Results: We determined that a hyperglycemic, low-serum, acidic medium stimulated TnT formation between all ovarian cancer cells studied, and more significantly, formed direct connections between A2780 to both C200 and SKOV3 cell lines. Conversely, Everolimus or Metformin decreased TnT formation in all cell lines with continuous exposure up to 96 hours; most prominently for the platinum-sensitive cell line. Time-lapse microscopy was used to assess chronologic formation of TnTs at the advancing front of the scratch wound. Cell proliferation assays were performed and confirmed the decrease in TnTs was not due to decreased cell proliferation. We directly observed fluorescing doxorubicin within the TnTs, suggesting TnTs act as a transport mechanism for cellular communication. Conclusions: TnT formation is stimulated in conditions of cellular stress similar to those experienced in vivo and results in direct connections between cells. Our data suggests that these conduits are a potential means of cellular exchange between platinum-sensitive and resistant ovarian cancer cells. Using currently available agents to target TnTs and disrupt this communication provides a novel approach to understanding and treating the problem of platinum resistance in ovarian cancer.

Effect of MicroRNA-210 on the Growth of Ovarian Cancer Cells and the Efficacy of Radiotherapy

2020 ◽  
pp. 1-10
Author(s):  
Yinlong Zhao ◽  
Shirui Liu ◽  
Yu Wen ◽  
Lili Zhong
Keyword(s):  
Ovarian Cancer ◽  
Cell Proliferation ◽  
Cancer Cells ◽  
Caspase 3 ◽  
Ovarian Cancer Cell ◽  
Migration And Invasion ◽  
Ovarian Cancer Cells ◽  
Over Expression ◽  
Proliferation Activity ◽  
Related Proteins

<b><i>Objective:</i></b> The objective of this study is to explore the role of miR-210 in the growth of ovarian cancer cells and the correlation with radiotherapy and to elucidate underlying molecular mechanisms. <b><i>Methods:</i></b> Human ovarian cancer cell lines OVCAR3 and SKOV3 were cultured in vitro, and miR-210 over-expression and low-expression ovarian cancer cell models were established by cell transfection. MTT assay was used to detect the proliferation activity. Transwell was used to detect the migration and invasion abilities. Western blot measured the expression of proteins related to cell proliferation, migration, and invasion. The cells were treated with different doses of ionizing radiation, and then the cell proliferation activity was detected by MTT. The expression of apoptosis-related proteins was detected by Western blot. The Caspase-Glo<sup>®</sup> Kit was used to detect the activity of cellular caspase 3/7 enzymes. <b><i>Results:</i></b> The proliferation, migration, and invasion abilities of miR-210 over-expression ovarian cancer cells were increased (<i>p</i> &#x3c; 0.05), the expressions of PTEN and E-cadherin were decreased, and the expression of p-Protein kinase B (AKT), N-cadherin, Snail, and Vimentin were elevated. After ionizing radiation, the sensitivity of miR-210 over-expression cells to radiotherapy was decreased, the expression of apoptosis-related protein Bax was decreased, the expression of Bcl-2 was increased, and the activity of cellular caspase 3/7 enzyme was reduced (<i>p</i> &#x3c; 0.05). <b><i>Conclusion:</i></b> miR-210 can promote the proliferation, migration, and invasion of ovarian cancer cells by activating the AKT signaling pathway and regulating the expression of Epithelial-mesenchymal transition-related proteins. miR-210 can reduce the sensitivity of ovarian cancer cells to radiotherapy by inhibiting apoptosis, which might serve as a potential target for the treatment of ovarian tumors.

Dihydromyricetin Inhibits Proliferation, Migration, and Invasion of Pancreatic Cancer Cells by Regulating miR-509-3p/PRMT5 Pathway

2021 ◽  
Vol 11 (3) ◽  
pp. 392-401
Author(s):  
Qiang Wang ◽  
Qichen Chai ◽  
Jin Chen ◽  
Jing Lv ◽  
Xiaofang Tang
Keyword(s):  
Pancreatic Cancer ◽  
Cell Proliferation ◽  
Protein Expression ◽  
Cyclin D1 ◽  
Cancer Cells ◽  
Inhibition Rate ◽  
Expression Levels ◽  
Pancreatic Cancer Cells ◽  
Proliferation And Metastasis ◽  
Sw1990 Cell

To explore the role of dihydromyricetin (DHM) in regulating proliferation, metastasis and infiltration of pancreatic cancer cells, we treated the pancreatic adenocarcinoma cell line SW1990 with 10 µmol/L, 20 µmol/L, and 40 µmol/L DHM. Proliferation was determined by the MTT assay. Cell metastasis and infiltration were determined by the Transwell migration assay. The protein expression levels of cyclin D1, p21, MMP-2, MMP-9, and PRMT5 were determined by Western blot. Quantitative PCR was used to determine expression of miR-509-3p and PRMT5 mRNA. The relationship between miR-509-3p and PRMT5 was analyzed by bioinformatic prediction and the dual luciferase reporter assay. SW1990 cells were transfected with miR-509-3p, si-PRMT5 and anti-miR-509-3p (following treatment with 40 µmol/L DHM) to determine their effects on biological behaviors of cells. The inhibition rate of SW1990 cells, p21 protein and miR-509-3p expression were increased by DHM. Moreover, the number of infiltrating and metastatic cells, protein levels of cyclin D1, MMP-2, MMP-9, and PRMT5, and mRNA levels of PRMT5 were decreased by DHM. miR-509-3p regulates expression of its target PRMT5 mRNA. Inhibition rate of SW1990 cell proliferation and protein level p21 were significantly increased by overexpression of miR-509-3p or knockdown of PRMT5 expression, while the number of invasive cells and protein expression levels of cyclin D1, MMP-2 and MMP-9 were remarkably reduced by miR-509-3p overexpression or PRMT5 knockdown. Inhibition of miR-509-3p counteract the inhibitory effects of DHM on SW1990 cell proliferation and metastasis. Therefore, DHM inhibits proliferation and metastasis of pancreatic carcinoma cells by regulating the miR-509-3p/PRMT5 pathway.

scholarly journals HOTAIR Interacting with MAPK1 Regulates Ovarian Cancer skov3 Cell Proliferation, Migration, and Invasion

2015 ◽  
Vol 21 ◽  
pp. 1856-1863 ◽  
Author(s):  
Tang Yiwei ◽  
Huang Hua ◽  
Guo Hui ◽  
Meng Mao ◽  
Long Xiang
Keyword(s):  
Ovarian Cancer ◽  
Cell Proliferation ◽  
Migration And Invasion ◽  
Skov3 Cell

scholarly journals Dezocine inhibits cell proliferation, migration and invasion by targeting CRABP2 in ovarian cancer

2020 ◽  
Author(s):  
Chuanfeng Zhang ◽  
Ruirui Pan ◽  
Shuangshuang Ma ◽  
Shoucai Xu ◽  
Baosheng Wang
Keyword(s):  
Ovarian Cancer ◽  
Cell Proliferation ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Ovarian Cancer Cell ◽  
Metastatic Potential ◽  
Migration And Invasion ◽  
Ovarian Cancer Cells ◽  
Mechanism Study ◽  
Skov3 Cells

Abstract Background Previous studies have shown that some anesthesia drugs can inhibit tumor growth and metastasis. As a clinical anesthetic drug, dezocine has been reported to play an important role in immune function. However, the effects of dezocine on ovarian cancer cell growth and metastasis are not fully understood. Results In this study, we found that dezocine dose-dependently inhibited the viability of ES-2 and SKOV3 cells. Dezocine suppressed the migration and invasion abilities of ovarian cancer cells, and promoted apoptosis. Moreover, the Akt/mTOR signaling pathway was also inhibited by dezocine. Furthermore, mechanism study showed that dezocine could significantly inhibited the expression of CRABP2, and CRABP2 overexpression reversed the inhibitory effects of dezocine on ovarian cancer cell proliferation and migration. Conclusion In conclusion, dezocine has significant anti-tumor effects on the growth and metastatic potential of ovarian cancer cells, and CRABP2 functions as a downstream effector of dezocine.

scholarly journals Involvement of Wnt/β-catenin pathway in the inhibition of invasion and epithelial-mesenchymal transition in ovarian cancer cells

2020 ◽  
Vol 19 (7) ◽  
pp. 1365-1370
Author(s):  
Belikiz Ekem ◽  
Wei Gong ◽  
Lu Han ◽  
Xinmei Wang ◽  
Na Liu ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Cell Proliferation ◽  
Cell Migration ◽  
Protein Expression ◽  
Signaling Pathway ◽  
Cell Invasion ◽  
Epithelial Mesenchymal Transition ◽  
Migration And Invasion ◽  
Mesenchymal Transition ◽  
Expression Levels

Purpose: To investigate the effects of zerumbone on cell invasion, epithelial-mesenchymal transition (EMT) and the potential signaling pathway involved in ovarian cancer cells.Methods: Caov-3 cell proliferation was assessed using 3-(4,5)-dimethylthiahiazo (-z-y1)-3,5-diphenytetrazoliumromide (MTT) assay. Wound healing assay was used to determine Caov-3 cell migration while cell invasion was evaluated using Transwell assay. Protein expression was determinedby western blot.Results: Cell viability was reduced by 5, 10, 20, and 50 μM zerumbone (p < 0.05) in a concentrationdependent manner while cell migration and invasion were inhibited by 10 and 20 μM zerumbone (p < 0.05). Protein expression levels of E-cadherin and cytoplasm β-catenin were upregulated by zerumbone (p < 0.05) in a concentration-dependent manner. On the other hand, protein expression levels of Ncadherin, vimentin, ZEB1, nuclear β-catenin, and c-Myc were suppressed by zerumbone (p < 0.05) also in a concentration-dependent manner.Conclusion: The results demonstrate that zerumbone inhibits cell proliferation, migration and invasion, but represses the EMT process via inactivation of Wnt/β-catenin signaling pathway. Keywords: Zerumbone, Ovarian cancer, Wnt/β-catenin pathway, Epithelial-mesenchymal transition

scholarly journals TUSC3 inhibits cell proliferation and invasion in cervical squamous cell carcinoma via suppression of the AKT signaling pathway

2021 ◽  
Author(s):  
Fei Sun ◽  
Qiuling Jie ◽  
Qi Li ◽  
Yunjian Wei ◽  
Ping Long ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Squamous Cell Carcinoma ◽  
Protein Expression ◽  
Cancer Cells ◽  
Signaling Pathway ◽  
Cervical Squamous Cell Carcinoma ◽  
Akt Signaling ◽  
Migration And Invasion ◽  
Akt Signaling Pathway ◽  
Proliferation And Invasion

Abstract Background The expression of tumor suppressor candidate 3 (TUSC3) is associated with proliferation in several types of cancer, leading to an unfavorable prognosis. The present study aimed to assess the cellular and molecular function of TUSC3 in patients with cervical squamous cell carcinoma (CSCC). Methods Levels of mRNA expressions of TUSC3 were analyzed in CSCC tissues and six cell lines using qRT-PCR. Immunohistochemistry(IHC) was used to evaluate the protein expression level of TUSC3 in four paired specimens, 220 paraffin-embedded CSCC specimens and 60 cases of normal cervical tissues(NCTs), respectively. Short hairpin RNA interference was employed for TUSC3 knockdown. Cell proliferation, migration and invasion was evaluated using growth curve, MTT assay, wound healing and transwell assay respectively. Results The results demonstrated that TUSC3 mRNA and protein expression levels were down-regulated in CSCC samples. Multivariate and univariate analyses indicated that TUSC3 was an independent prognostic factor for patients with CSCC. Decreased TUSC3 expression levels were significantly associated with proliferation and an aggressive phenotype of cervical cancer cells. Moreover, the knockdown of TUSC3 promoted migration and invasion of cancer cells, while the increased expression of TUSC3 exhibited the opposite effects. The down-regulation of TUSC3 facilitated proliferation and invasion of CSCC cells through the activation of the AKT signaling pathway. Conclusions Our data demonstrated that the down-regulation of TUSC3 promoted CSCC cell metastasis via the AKT signaling pathway. Therefore, TUSC3 may serve as a novel prognostic marker and potential target for CSCC.

scholarly journals Exosome Component 4 Promotes Epithelial Ovarian Cancer Cell Proliferation, Migration, and Invasion via the Wnt Pathway

2021 ◽  
Vol 11 ◽  
Author(s):  
Chang Xiong ◽  
Zhongfeng Sun ◽  
Jinjin Yu ◽  
Yaying Lin
Keyword(s):  
Ovarian Cancer ◽  
Protein Expression ◽  
Epithelial Ovarian Cancer ◽  
Cyclin D1 ◽  
Cell Lines ◽  
Wnt Pathway ◽  
Migration And Invasion ◽  
Mrna Levels ◽  
Expression Levels ◽  
E Cadherin

BackgroundOf gynecologic malignancies, ovarian cancer is the leading cause of death, mainly due to the lack of sensitive tumor markers, which means it almost always presents at an advanced stage. Exosome Component 4 (EXOSC4) is involved in RNA degradation, but its role in epithelial ovarian cancer (EOC) is unclear.MethodsThe expression levels of EXOSC4 in EOC and normal ovarian tissue specimens were determined by immunohistochemical staining. The overall survival (OS) and progression-free survival (PFS) of patients with EOC were evaluated after patients were classified into high and low EXOSC4 expression groups, and the Cox regression model was established to identify independent predictors of patient prognosis. The effects of EXOSC4 on proliferation, colony formation, migration, and invasion were examined in the SKOV-3 and HO8910 cell lines by lentivirus-mediated shRNA knockdown. Flow cytometry was used to detect cell cycle changes. The mRNA levels of cyclin D1, CDK4, and c-myc were detected by RT-PCR. The protein expression levels of β-catenin, cyclin D1, CDK4, c-myc, vimentin, N-cadherin, and E-cadherin were assessed by western blot. Wnt/β-catenin activation was measured by TCF/LEF reporter assay.ResultsEXOSC4 was significantly elevated in EOC tissues and cell lines. High EXOSC4 expression was correlated with the International Federation of Gynecology and Obstetrics (FIGO) stage and pathological grade, and identified as an independent predictor of shorter OS and PFS. EXOSC4 knockdown suppressed proliferation, migration, and invasion in EOC cell lines. Cells were arrested at G0/G1 phase after EXOSC4 knockdown. The mRNA levels of cyclin D1, CDK4, and c-myc were decreased. β-catenin, cyclin D1, CDK4, c-myc, vimentin, and N-cadherin protein expression levels were reduced, while those of E-cadherin was increased. Wnt/β-catenin activity was suppressed after the EXOSC4 knockdown.ConclusionsEXOSC4 is involved in EOC. Knockdown of EXOSC4 can inhibit the proliferation, migration, and invasion ability of EOC by suppressing the Wnt pathway. EXOSC4 is expected to be a novel biomarker and molecular target in EOC.

Vitamin C supplementation had no side effect in non-cancer, but had anticancer properties in ovarian cancer cells

2020 ◽  
pp. 1-11 ◽  
Author(s):  
Ewa Lucja Gregoraszczuk ◽  
Karolina Zajda ◽  
Joanna Tekla ◽  
Natalia Respekta ◽  
Paweł Zdybał ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Cell Proliferation ◽  
Vitamin C ◽  
Protein Expression ◽  
Cancer Cells ◽  
Basal Medium ◽  
Ovarian Cancer Cells ◽  
Cyclin Dependent Kinase ◽  
Apoptosis Pathway ◽  
Vit C

Abstract. Vitamin C (Vit C) has been widely used in the treatment and prevention of cancer. Nevertheless, the clinical results are still inconclusive. Using non-cancer (HOSEpiC) and cancer OVCAR-3 cells cultured in basal medium or in ovarian cancer-associated fibroblast (CAF)-supplemented medium, we estimated the dose-dependent effect of Vit C on sodium–ascorbate co -transporters (SVCT1, SVCT2) and g lucose transporter (GLUT1) protein expression. Additionally, the action of Vit C on cell proliferation (alamarBlue), membrane permeability (LDH assay), caspase3 activity, the selected cell cycle and apoptosis pathway, poly(ADP-ribose) polymerase-1 (PARP) protein expression, and reactive oxygen species (ROS) activity was determined. We showed different effects of Vit C on the expression of the co-transporter in non-cancer and cancer cells. In non-cancer cells, Vit C, at a pharmacological concentration, increased SVCT2 and decreased GLUT1, while the opposite effect was noted in cancer cells. In cancer cells, Vit C, in a pharmacological dose, decreased cell proliferation through an inhibitory effect on cyclin-dependent kinase 2 (CDK2) (4.4-fold; p < 0.01), mainly due to the stimulatory effect on the expression of cyclin-dependent kinase (CDK) inhibitors, such as p21 and p53 (3.2- and 2.8-fold, respectively; p < 0.001), but not caspase pathway. The tumour microenvironment caused inefficiency of the lower doses of Vit C in ovarian cancer cells. At a pharmacological dose of 1 mM, Vit C decreased PARP expression (1.5-fold; p < 0.05). We suggest that it’s nontoxic effects on non-cancer cells may be an indicator of its prophylactic use, while in a pharmacological dose Vit C should be considered a possible adjunctive drug in ovarian cancer. However, it is necessary to consider the effect of the CAF.

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