scholarly journals Alkannin Inhibits the Development of Ovarian Cancer by Affecting miR-4461

2021 ◽  
Vol 2021 ◽  
pp. 1-8
Author(s):  
Yaowen Wang ◽  
Jingfang Zhang ◽  
Feipeng Wang ◽  
Wenping Chen ◽  
Jie Ma ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Flow Cytometry ◽  
Cell Viability ◽  
Migration And Invasion ◽  
Flow Cytometry Analysis ◽  
Antibacterial Effects ◽  
Transwell Assay ◽  
Ovarian Cells ◽  
Mrna And Protein Expression ◽  
Inhibit Cell Proliferation

Background. Previous studies have shown that alkannin has anticancer, anti-inflammatory, and antibacterial effects. However, the effect of alkannin in the development of ovarian cancer (OC) remains unknown. Therefore, this study aims to elucidate the function of alkannin in OC progression. Methods. RT-qPCR and western blot analysis were used to measure mRNA and protein expression. Cell viability and metastasis were detected by the CCK-8 assay, flow cytometry analysis, and transwell assay. Results. Alkannin had no cytotoxicity toward normal ovarian cells, but alkannin can inhibit cell proliferation and induce apoptosis in OC cells. In addition, alkannin inhibited cell migration and invasion and blocked EMT in OC. Besides, upregulation of miR-4461 was found in OC tissues and cells, which was regulated by alkannin. More importantly, miR-4461 can inverse the effects of alkannin on cell viability and metastasis in OC cells. Conclusion. Alkannin restrains cell viability, metastasis, and EMT in OC by downregulating miR-4461 expression.

scholarly journals Expression of SASH1 in Preeclampsia and Its Effects on Human Trophoblast

2020 ◽  
Vol 2020 ◽  
pp. 1-8
Author(s):  
Shisan Liu ◽  
Sijia Jiang ◽  
Liping Huang ◽  
Yanhong Yu
Keyword(s):  
Flow Cytometry ◽  
Matched Control ◽  
Migration And Invasion ◽  
Flow Cytometry Analysis ◽  
Vector Group ◽  
Transwell Assay ◽  
Human Trophoblast ◽  
Empty Vector ◽  
Group Flow

Aim. To explore the involvement of SASH1 in preeclampsia. Methods. Expression of SASH1 was determined by qPCR, WB, and immunohistochemistry in the placenta of both normal and preeclamptic pregnancies. The SASH1 gene of human HTR-8/SVneo cells was overexpressed by transfection of pEZ-Lv206-SASH1. After that, the CCK-8 assay, EdU assay, transwell assay, and flow cytometry were used to examine the cell proliferation, migration, invasion, and apoptosis. Results. Higher expression of SASH1 was detected in placental tissues collected from patients with preeclampsia, compared with those from gestational age-matched control samples. The expression of SASH1 was significantly enhanced by transfection with pEZ-Lv206-SASH1 in HTR-8/SVneo cells. In addition, the HTR-8/SVneo cells transfected with pEZ-Lv206-SASH1 exhibited significantly reduced proliferation, migration, and invasion ability compared to the cells in the empty vector group and normal group. Flow cytometry analysis demonstrated that the apoptosis rate of cells transfected with pEZ-Lv206-SASH1 was significantly higher than that of cells transfected with empty vector and untreated cells. Conclusions. SASH1 is significantly upregulated in the placenta of preeclampsia, and overexpression of SASH1 can inhibit the proliferation, migration, and invasion, but induce apoptosis of trophoblast cells in vitro.

LncRNA SNHG14 Promotes Progression of Ovarian Cancer by Regulating miR-206 Expression

2021 ◽  
Vol 7 (5) ◽  
pp. 3997-4004
Author(s):  
Zhibo Zou ◽  
Lin Peng
Keyword(s):  
Ovarian Cancer ◽  
Flow Cytometry ◽  
Cell Proliferation ◽  
Tumor Growth ◽  
Cancer Progression ◽  
Nude Mice ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Qrt Pcr ◽  
Research Objects

Objective: This study aimed to probe into the effect of LncRNA SNHG14 on ovarian cancer progression by regulating miR-206.Methods: Fifty-seven ovarian cancer (OC) patients who were treated in our hospital from December 2017 to December 2019 were collected as the research objects. During the operation, OC tissues and paracancerous tissues of patients were collected, and the effect of SNHG14 on OC tumor growth in nude mice was detected, and SNHG14 inhibitor was transfected into OC cells. The relative expression of SNHG14 in tissues and cells was detected by qRT-PCR, cell proliferation was testedvia CCK8, migration and invasion were detected through Transwell, apoptosis was assessedvia flow cytometry, and the targeted relationship between SNHG14 and miR-206 was detected by dual luciferase reporter gene.Results: SNHG14 is highly expressed in OC tissues, cells and nude mice. Down-regulating it can inhibit the biological ability of OC cells and inhibit the growth of nude mice tumors. It can directly target miR-206 to regulate CCND1 expression and promote OC progression.Conclusion: LncRNA SNHG14 can act as miR-206 sponge to regulate CCND1 expression downstream of miR-206 and promote OC progression.

Silencing of lncRNA MEG8 Represses the Viability, Migration, and Invasion of Wilms’ Tumor Cells through Mediating miR-23a-3p/CRK Axis

2021 ◽  
pp. 1-13
Author(s):  
Jing Shen ◽  
Qiang Shu
Keyword(s):  
Cell Viability ◽  
Wilms Tumor ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Transwell Assay ◽  
Reaction Cell ◽  
Tumor Study ◽  
Polymerase Chain ◽  
Dual Luciferase Reporter Assay

<b><i>Purpose:</i></b> Compelling evidence has unveiled the importance of long noncoding RNAs (lncRNAs) in malignant behavior of Wilms’ tumor (WT). Hereon, we intend to assess the function and associated molecular mechanism of lncRNA maternally expressed gene 8 (MEG8) in WT cells. <b><i>Methods:</i></b> Expression levels of MEG8, miR-23a-3p, and CT10 regulator of kinase (CRK) were determined by quantitative real-time polymerase chain reaction. Cell viability was assessed by MTT assay. Besides, wound healing assay and transwell assay were applied to examine abilities of cell migration and invasion, respectively. Dual-luciferase reporter assay was employed to test the interplay among MEG8, miR-23a-3p, and CRK. Western blot was used to detect relative protein expression of CRK. <b><i>Results:</i></b> MEG8 and CRK expression was elevated, while miR-23a-3p expression was decreased in WT tissues and cells. The histologic type, lymphatic metastasis, and National Wilms Tumor Study (NWTS) stage were associated with the expression of MEG8, miR-23a-3p, and CRK in WT patients. MEG8 knockdown or miR-23a-3p overexpression restrained WT cells in cell viability, migration, and invasiveness in vitro. As to mechanism exploration, MEG8 could directly bind to miR-23a-3p and then miR-23a-3p targeted CRK. MEG8 was inversely correlated with miR-23a-3p and positively correlated with CRK in WT tissues. Meantime, miR-23a-3p was inversely correlated with CRK in WT tissues. Additionally, MEG8 knockdown-mediated suppressive impacts on cell viability, migration, and invasiveness were reversed by overexpression of CRK or repression of miR-23a-3p in WT cells. <b><i>Conclusions:</i></b> The cell viability, migration, and invasiveness of WT cells were repressed by MEG8 knockdown via targeting the miR-23a-3p/CRK axis.

Flow Cytometry Analysis of G0/G1 Diploid Cell Fraction in Ovarian Cancer Tissue

2018 ◽  
Vol 73 (5) ◽  
pp. 244-247
Author(s):  
T. A. Bogush ◽  
I. A. Mamichev ◽  
Iu. P. Borisenko ◽  
E. A. Bogush ◽  
N. O. Vichljantseva ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Flow Cytometry ◽  
Diploid Cell ◽  
Cell Fraction ◽  
Cancer Tissue ◽  
Flow Cytometry Analysis ◽  
Ovarian Cancer Tissue

ZEB1 Promotes Chemoresistance to Cisplatin in Ovarian Cancer Cells by Suppressing SLC3A2

Chemotherapy ◽  
2018 ◽  
Vol 63 (5) ◽  
pp. 262-271 ◽  
Author(s):  
Yajie Cui ◽  
Li Qin ◽  
Defu Tian ◽  
Ting Wang ◽  
Lijing Fan ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Cell Viability ◽  
Cancer Cells ◽  
Tumor Development ◽  
Migration And Invasion ◽  
Ovarian Cancer Cells ◽  
Cell Surface Molecule ◽  
Important Regulator ◽  
Induced Apoptosis

Ovarian cancer is one of the deadliest gynecological malignancies in women. Chemoresistance has been a major obstacle for ovarian cancer treatment. Zinc finger E-box-binding homeobox 1 (ZEB1) is an important regulator of tumor development in various types of cancer. Abnormal expression of SLC3A2 (CD98hc), a type 2 transmembrane cell surface molecule, has been described in several cancers. This study was designed to investigate the role of ZEB1 and SLC3A2 in the chemoresistance to cisplatin in ovarian cancer cells. We found that ZEB1 was increased in cisplatin-resistant SKOV3/DPP cells. Downregulation of ZEB1 significantly decreased cell viability in response to cisplatin, increased cis­platin-induced apoptosis, and decreased migration and invasion in the presence of cisplatin. In addition, downregulation of ZEB1 decreased the volume and weight of implanted tumors. SLC3A2 was decreased in cisplatin-resistant SKOV3/DPP cells. Upregulation of SLC3A2 significantly decreased cell viability in response to cisplatin, increased cisplatin-induced apoptosis, and decreased migration and invasion in the presence of cisplatin. Moreover, upregulation of SLC3A2 decreased the volume and weight of implanted tumors. Downregulation of ZEB1 resulted in a significant increase of SLC3A2 expression. Moreover, downregulation of SLC3A2 significantly inhibited ZEB1 knockdown-mediated inhibition of cisplatin-resistance. ZEB1-mediated regulation of SLC3A2 was involved in the chemoresistance to cisplatin in ovarian cancer cells. Overall, we provide new insights into the mechanism of chemoresistance to cisplatin in ovarian cancer cells. ZEB1/SLC3A2 may be promising therapeutic targets for enhancement of the sensitivity of ovarian cancer cells to cisplatin-mediated chemotherapy.

Propranolol induced apoptosis and autophagy via the ROS/JNK signaling pathway in human ovarian cancer

2020 ◽  
Author(s):  
Shujun Zhao ◽  
Suzhen Fan ◽  
Yanyu Shi ◽  
Hongyan Ren ◽  
Hanqing Hong ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Flow Cytometry ◽  
Signaling Pathway ◽  
Cell Apoptosis ◽  
Human Ovarian Cancer ◽  
Dependent Manner ◽  
Flow Cytometry Analysis ◽  
Jnk Signaling ◽  
Jnk Signaling Pathway ◽  
Induced Apoptosis

Abstract Background: Propranolol has a significant anti-cancer effect on various cancers. The present study aimed to investigate the underlying mechanism behind the therapeutic effect of Propranolol on the ovarian cancer.Materials and methods: The effect of Propranolol on cell viability was examined by MTT analysis. Cellular apoptosis was evaluated by flow cytometry analysis. Autophagy was defined by autophagosome observed by confocal microscopy after infected with GFP-LC3 adenovirus. In addition, the expression of marker proteins involved in cell apoptosis, autophagy, and ROS/JNK signaling pathway were estimated by Western Blotting assay.Results: Propranolol significantly reduced the viability of human ovarian cancer cell lines SKOV-3 and A2780 in a dose- and time-dependent manner. Flow cytometry analysis revealed that Propranolol induced the cell cycle arrest at G2/M phase and resulted in apoptosis. Moreover, autophagy inhibitor 3-MA markedly enhanced the Propranolol-induced apoptosis. In addition, reactive oxygen species (ROS) was demonstrated dramatically increased after Propranolol treatment and Propranolol activated the phosphorylation of JNK. What is more, p38 inhibitor SB203580 and JNK inhibitor SP600125 attenuated the upregulated expression of LC3-II and cleaved-caspase-3 by the effect of Propranolol. ROS exclusive inhibitor antioxidant N-acetyl cysteine (NAC) weaken the phosphorylation of JNK proteins induced by Propranolol.Conclusions：In summary, our results suggested that Propranolol induced cell apoptosis and protective autophagy through the ROS/JNK signaling pathway in human ovarian cancer cells.

scholarly journals Higher Numbers of T-Bet+ Tumor-Infiltrating Lymphocytes Associate with Better Survival in Human Epithelial Ovarian Cancer

2017 ◽  
Vol 41 (2) ◽  
pp. 475-483 ◽  
Author(s):  
Yun Xu ◽  
Lujun Chen ◽  
Bin Xu ◽  
Yuqi Xiong ◽  
Min Yang ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Flow Cytometry ◽  
Epithelial Ovarian Cancer ◽  
Cancer Patients ◽  
Tumor Infiltrating Lymphocytes ◽  
Lymphoid Cells ◽  
Type I ◽  
Flow Cytometry Analysis ◽  
Cancer Tissues ◽  
Infiltrating Lymphocytes

Background/Aims: T-bet, a member of the T-box family of transcription factors, is a key marker of type I immune response within the tumor microenvironment, and has been previously reported by us to serve as an important prognostic indicator for human gastric cancer patients and a potential biomarker for immunotherapy. In the present study, we aimed to assess the clinical significance and prognostic value of T-bet+ tumor-infiltrating lymphocytes in human epithelial ovarian cancer. Methods: The immunohistochemistry was used to analyze the infiltration density of T-bet+ lymphoid cells in human epithelial ovarian cancer tissues, and the flow cytometry analysis was used to further analyze the presence of T-bet+ tumor-infiltrating lymphocytes subgroups in cancer tissues. Results: Our immunohistochemistry analysis showed increased number of T-bet+ lymphoid cells in the human epithelial ovarian cancer tissues, and the flow cytometry analysis further demonstrated the presence of T-bet+ tumor-infiltrating lymphocytes subgroups including CD4+ , CD8+ T cells and NK cells. In addition, we also observed a significant association of T-bet+ tumor-infiltrating lymphocytes density in the tumor nest of cancer with not only serum CA125 levels but also with distant metastasis. However no association was observed with other characteristics like patients' age, pathological type, FIGO stage, tumor site and tumor size. Furthermore, the survival analysis showed that higher density of T-bet+ tumor-infiltrating lymphocytes both in tumor nest and tumor stroma of cancer tissues was significantly associated with better patient survival. In addition, the density of T-bet+ tumor-infiltrating lymphocytes in tumor nest appeared to be an independent risk factor for predicting patients’ postoperative prognoses. Conclusions: Our data indicated that the key transcription factor T-bet might play an important role in the type I immune cells mediated antitumor response, and the density of T-bet+ lymphocytes in human epithelial ovarian cancer tissues could serve as a prognostic predictor for ovarian cancer patients.

scholarly journals Long non-coding RNA NEAT1/miR-320b/MSI2 axis regulates cisplatin resistance in ovarian cancer

2021 ◽  
Author(s):  
Chunling Zhao ◽  
Pingfen Zi ◽  
Degang Zhou
Keyword(s):  
Ovarian Cancer ◽  
Cell Viability ◽  
Cisplatin Resistance ◽  
Cell Counting ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Novel Therapy ◽  
Non Coding Rna ◽  
Long Non Coding Rna

IntroductionOvarian cancer (OC) frequently occurs in postmenopausal women and it has higher mortality rate. Accumulating researches proved that long non-coding RNA nuclear paraspeckle assembly transcript 1 (NEAT1) involved in the progression of chemoresistance in human OC. Here, the study aimed to investigate the partial molecular mechanism of OC chemoresistance.Material and methodsThe levels of NEAT1 and microRNA-320b (miR-320b) were measured by qRT-PCR. Western blot was carried out to determine the protein levels that used in this research. Cell viability was identified via Cell Counting Kit-8 (CCK-8). Transwell assay was employed to determine migration and invasion. The relationship between miR-320b and NEAT1 or MSI2 was clarified by dual-luciferase reporter assay, RNA immunoprecipitation (RIP) and RNA pull down assay. Also, a murine xenograft assay was used to explore the effect of NEAT1 on cisplatin resistance in OC in vivo.ResultsThe level of NEAT1 was significantly increased in cisplatin resistant OC cell lines. Downregulation of NEAT1 enhanced cisplatin sensibility in OVCAR-3/DDP and HEY/DDP cells. Furthermore, miR-320b was a target of NEAT1, and the effects of knockdown of NEAT1 on the cell viability, IC50 of cisplatin, migration and invasion in OVCAR-3/DDP and HEY/DDP were restored by the inhibitor of miR-320. In addition, miR-320b directly targeted MSI2 to regulate cisplatin sensibility in cisplatin resistant OC cells. In addition, downregulation of NEAT1 decreased cisplatin resistance in OC in vivo.ConclusionsNEAT1 regulated cisplatin resistance through NEAT1/miR-320b/MSI2 axis in OC, which might offer a novel therapy target for the chemotherapy of OC.

scholarly journals Sevoflurane but not propofol enhances ovarian cancer cell malignancy through regulating cellular metabolic and signalling mechanisms

2021 ◽  
Author(s):  
Cong Hu ◽  
Bincheng Wang ◽  
Zhigang Liu ◽  
Qiling Chen ◽  
Masashi Ishikawa ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Cell Viability ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Ovarian Cancer Cell ◽  
Cell Counting ◽  
Immunofluorescent Staining ◽  
Migration And Invasion ◽  
Ovarian Cancer Cells ◽  
Cellular Signalling

Background and Purpose: Surgery remains the first-line treatment of ovarian cancer. However, perioperative risk factors including the choice of anaesthetics may influence its recurrence after surgery. In the current study, it was hypothesised that inhalational anaesthetic sevoflurane and intravenous anaesthetic propofol might affect cancer cellular metabolism and signalling, which might interfere the malignancy of ovarian cancer cells. Experimental Approach: Cultured ovarian cancer cells were exposed to 2.5% sevoflurane or administered with 4 μg/mL propofol for 2 hours followed by 24 hours recovery. Their cell viability, proliferation, migration and invasion were assessed using cell counting kit-8, Ki-67 staining, wound healing and Transwell assay. Cellular signalling biomarkers were measured using immunofluorescent staining and/or Western blot. Cultured media were collected for 1H-NMR spectroscopy-based metabolomics analysis. Key Results: The cell viability, proliferation, migration, and invasion of ovarian cancer cells were enhanced by sevoflurane but suppressed by propofol. Sevoflurane increased the GLUT1, MPC1, GLUD1, p-Erk1/2, and HIF-1α expressions but decreased the PEDF expression. In contrast to the sevoflurane treatment, the “mirror changes” of these cellular markers were observed with propofol. Sevoflurane increased levels of isopropanol but decreased glucose and glutamine levels in the media, but the opposite changes of those metabolites were found after propofol treatment. Conclusion and Implications: These data indicated that unlike propofol, sevoflurane enhanced ovarian cancer cell metabolism and activated PEDF/Erk/HIF-1α cellular signalling pathway, suggesting that sevoflurane might have pro-tumour property but propofol might afford an anti-tumour property. The translational value of this work warrants further study.

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