New Blocking Antibodies Impede Adhesion, Migration and Survival of Ovarian Cancer Cells, Highlighting MFGE8 as a Potential Therapeutic Target of Human Ovarian Carcinoma

The encapsulation process of the PdII complex [PdCl(PPh3)(PrCh)], a promising cytotoxic agent on ovarian cancer cells, in PLGA polymer was studied. The cytotoxicity results showed that the formulation led to a significant reduction of the ovarian cell viability (80% at 1 μM).

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Theaflavin-3,3′-Digallate Suppresses Human Ovarian Carcinoma OVCAR-3 Cells by Regulating the Checkpoint Kinase 2 and p27 kip1 Pathways

Molecules ◽

10.3390/molecules24040673 ◽

2019 ◽

Vol 24 (4) ◽

pp. 673 ◽

Cited By ~ 3

Author(s):

Ying Gao ◽

Junfeng Yin ◽

Youying Tu ◽

Yi Chen

Keyword(s):

Ovarian Cancer ◽

Ovarian Carcinoma ◽

Cancer Cells ◽

Black Tea ◽

Ovarian Cancer Cells ◽

Human Ovarian Cancer ◽

Checkpoint Kinase ◽

Checkpoint Kinase 2 ◽

Human Ovarian Carcinoma ◽

P27 Kip1

Theaflavin-3,3′-digallate (TF3) is a unique polyphenol in black tea. Epidemiological studies have proved that black tea consumption decreases the incidence rate of ovarian cancer. Our former research demonstrated that TF3 inhibited human ovarian cancer cells. Nevertheless, the roles of checkpoint kinase 2 (Chk2) and p27 kip1 (p27) in TF3-mediated inhibition of human ovarian cancer cells have not yet been investigated. In the current study, TF3 enhanced the phosphorylation of Chk2 to modulate the ratio of pro/anti-apoptotic Bcl-2 family proteins to initiate intrinsic apoptosis in a p53-independent manner and increased the expression of death receptors to activate extrinsic apoptosis in OVCAR-3 human ovarian carcinoma cells. In addition, TF3 up-regulated the expression of p27 to induce G0/G1 cell cycle arrest in OVCAR-3 cells. Our study indicated that Chk2 and p27 were vital anticancer targets of TF3 and provided more evidence that TF3 might be a potent agent to be applied as adjuvant treatment for ovarian cancer.

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

RSC Advances ◽

10.1039/c9ra03783g ◽

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.

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BRCA1 Expression is an Important Biomarker for Chemosensitivity: Suppression of BRCA1 Increases the Apoptosis via Up-regulation of p53 and p21 during Cisplatin Treatment in Ovarian Cancer Cells

Biomarker Insights ◽

10.1177/117727190600100007 ◽

2006 ◽

Vol 1 ◽

pp. 117727190600100 ◽

Cited By ~ 2

Author(s):

Akiko Horiuchi ◽

Cuiju Wang ◽

Norihiko Kikuchi ◽

Ryosuke Osada ◽

Toshio Nikaido ◽

...

Keyword(s):

Ovarian Cancer ◽

Ovarian Carcinoma ◽

Cancer Cells ◽

Cell Lines ◽

Brca1 Gene ◽

Fold Increase ◽

Ovarian Cancer Cells ◽

Cancer Syndrome ◽

Brca1 Expression ◽

Skov3 Cells

BRCA1 is a tumor suppressor which plays a crucial role in the repair of DNA double-strand breaks, and its abnormality is responsible for hereditary ovarian cancer syndrome. It has recently been reported that reduced expression of BRCA1 is also common in sporadic ovarian carcinoma via its promoter hypermethylation, and that ovarian carcinoma patients negative for BRCA1 expression showed favorable prognosis. To address if BRCA1 expression plays a role in the chemotherapeutic response, we analyzed the effect of BRCA1 suppression on the sensitivity to cisplatin and paclitaxel in ovarian cancer cells. Specific siRNA for BRCA1 gene was transfected into 3 ovarian cancer cell lines with various p53 status. Reduced expression of BRCA1 by transfection of BRCA1-siRNA resulted in a 5.3-fold increase in sensitivity to cisplatin in p53-wild A2780 cells, but not in p53-mutated A2780/CDDP and p53-deleted SKOV3 cells. Regarding the sensitivity to paclitaxel, BRCA1 suppression caused no significant changes in all the 3 cell lines. For ionizing radiation sensitivity, BRCA1 suppression also showed a significant higher sensitivity in A2780 cells. Growth curve and cell cycle analyses showed no significant differences between BRCA1-siRNA-transfected A2780 cells and control cells. However, cisplatin treatment under suppression of BRCA1 showed a significantly increased apoptosis along with up-regulation of p53 and p21 in A2780 cells. Accordingly, reduced expression of BRCA1 enhances the cisplatin sensitivity and apoptosis via up-regulation of p53 and p21, but does not affect the paclitaxel sensitivity. Expression of BRCA1 might be an important biomarker for cisplatin resistance in ovarian carcinoma.

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Non-oncogenic deletion mutants of adenoviral E1A enhance paclitaxel induced apoptosis of ovarian cancer cells

Journal of Clinical Oncology ◽

10.1200/jco.2007.25.18_suppl.14102 ◽

2007 ◽

Vol 25 (18_suppl) ◽

pp. 14102-14102

Author(s):

C. Kurzeder ◽

C. Hanselmann ◽

N. DeGregorio ◽

G. Sauer ◽

B. Opalka ◽

...

Keyword(s):

Ovarian Cancer ◽

Gene Therapy ◽

Ovarian Carcinoma ◽

Cancer Cells ◽

Expression System ◽

Substantial Reduction ◽

Ovarian Cancer Cells ◽

Binding Motif ◽

Therapeutic Effects ◽

Induced Apoptosis

14102 Background: The phenotypical characteristics and spread of ovarian cancer cells, suggest intraperitoneal gene therapy of this disease. Phase I trials have been conducted to investigate the potential clinical benefits of adenoviral E1A-based gene therapy. Further gene therapeutic approaches which aim to enhance the efficacy of E1A-induced apoptosis in a multimodal approach including conventional chemotherapy are planned. However, besides tumor-suppressive effects, E1A is also known to transform rodent cells in conjunction with other factors, e.g. an activated ras oncogene. In an effort to eliminate elements favouring malignant conversion, the potential therapeutic effect of the E1AdelCR2 deletion mutant on ovarian cancer cells was studied. Methods: To avoid any selection bias, a doxycyclin-regulated system was used to express E1A wildtype protein and the mutant E1AdelCR2 lacking the p105RB-binding motif. The effects of the E1A proteins on proliferation and induction of apoptosis in ovarian carcinoma cell lines was studied with a WST-1 assay and fluorcytometric analysis of FITC labelled AnnexinV. Results: As confirmed by Western blot analyses, expression of the mutant proteins was almost completely suppressed in the presence of doxycyclin. Substantial reduction in proliferation was achieved by expression of both wildtype E1A and E1AdelCR2. Expression of E1AdelCR2 was sufficient by itself to induce apoptosis in 8,7% of ovarian carcinoma cells as shown by an increase of the fraction of Annexin binding OVMZ-8 cells. A strong synergistic effect with an increase of the fraction of apoptotoc cells by 16.7% was found when the cells were treated with paclitaxel. Conclusion: Deletion of the CR2 sequence should increase the safety of therapeutic applications of E1A without affecting tumor suppression. A doxycyclin-regulated expression system was established allowing the elucidation of the mechanisms underlying the therapeutic effects of E1A in ovarian cancer cells in the future by means of expression profiling and quantification of activated components of signal transduction pathways. No significant financial relationships to disclose.

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

10.21203/rs.3.rs-20826/v2 ◽

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.

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

Dalton Transactions ◽

10.1039/c9dt02894c ◽

2019 ◽

Vol 48 (34) ◽

pp. 13081-13093 ◽

Cited By ~ 6

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.

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Outcome in serous ovarian cancer is not associated with LATS expression

Journal of Cancer Research and Clinical Oncology ◽

10.1007/s00432-019-03037-4 ◽

2019 ◽

Vol 145 (11) ◽

pp. 2737-2749 ◽

Cited By ~ 4

Author(s):

Céline Montavon ◽

Gregor R. Stricker ◽

Andreas Schoetzau ◽

Viola Heinzelmann-Schwarz ◽

Francis Jacob ◽

...

Keyword(s):

Ovarian Cancer ◽

Protein Expression ◽

Ovarian Carcinoma ◽

Cancer Cells ◽

Drug Sensitivity ◽

Ovarian Cancer Cells ◽

Data Sets ◽

Serous Ovarian Cancer ◽

Transcriptomic Data ◽

Poor Outcome

Abstract Background Large tumor suppressor (LATS) proteins are putative tumor suppressors and poorly expressed associated with poor outcome in many cancers. A recent immunohistochemistry study showed that LATS protein expression correlated with poor outcome in serous ovarian cancer. Materials and methods We analyzed LATS expression in various ovarian cancer transcriptomic data sets and immunohistochemically assessed LATS protein expression in a Swiss ovarian tumor cohort. Results were compared to clinicopathological characteristics and outcome. We also compared LATS protein expression in serous ovarian cancer cell lines to their EMT status (Western blotting) and drug sensitivity (MTT assay). Results The analysis of 15 different transcriptomic data sets showed that LATS2 was associated with poorer outcome, while LATS1 was irrelevant (HR = 1.19 and HR = 1.00, respectively). The TCGA-RNASeqV2 data set showed that low LATS1 and LATS2 were associated with better survival in serous ovarian carcinoma. Despite heterogeneity among the different data sets, LATS expression is not an indicator of survival in serous ovarian cancer and LATS2 expression may even be tumorigenic. LATS expression was neither associated with survival nor with the stage and grade in the Swiss cohort. It was low in cystadenoma, intermediate in carcinoma, and high in borderline tumors and was higher in serous than mucinous ovarian carcinoma. LATS protein expression extent was comparable in epithelial-, intermediate-, and mesenchymal-type ovarian cancer cells and was not associated with drug sensitivity. Conclusion These results are largely incompatible with a tumor-suppressive function of LATS in ovarian cancer, and LATS protein level is also not an indicator for drug sensitivity and EMT status of ovarian cancer cells.

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Effects of celastrol on enhancing apoptosis of ovarian cancer cells via the downregulation of microRNA-21 and the suppression of the PI3K/Akt-NF-κB signaling pathway in an in vitro model of ovarian carcinoma

Molecular Medicine Reports ◽

10.3892/mmr.2016.5894 ◽

2016 ◽

Vol 14 (6) ◽

pp. 5363-5368 ◽

Cited By ~ 11

Author(s):

Haiyan Zhang ◽

Jianhua Li ◽

Guang Li ◽

Surong Wang

Keyword(s):

Ovarian Cancer ◽

Ovarian Carcinoma ◽

Cancer Cells ◽

Signaling Pathway ◽

In Vitro Model ◽

Ovarian Cancer Cells ◽

Vitro Model

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LPA3 Is a Precise Therapeutic Target And Potential Biomarker For Ovarian Cancer

10.21203/rs.3.rs-875460/v1 ◽

2021 ◽

Author(s):

Pengfei Zhao ◽

Qingru Yun ◽

Aodungerile Li ◽

Rong Li ◽

Yali Yan ◽

...

Keyword(s):

Ovarian Cancer ◽

Cancer Cells ◽

Therapeutic Target ◽

Bioinformatic Analysis ◽

Ovarian Cancer Cells ◽

Cancer Tissue ◽

Lpa Receptor ◽

Ovarian Cancer Tissue ◽

Potential Biomarker

Abstract Current studies have demonstrated that significant increased LPA levels to be observed in ascites in patients with ovarian cancer. Although several studies have shown that Lysophosphatidic acid (LPA) related to the progression of ovarian cancer, which LPA receptors (LPARs) and G coupled protein subtypes mediated in LPA actions have not been clearly elucidated. This study aimed to clarify the roles of LPA and it’s subtype-specific LPARs mediating mechanisms in ovarian cancer by integrated using bioinformatic analysis and biological experimental approaches. The big data analysis shown that LPA3 was the only differentially expressed LPA receptor among the six LPARs in ovarian cancer and further verified in immunohistochemistry of tissue microarrays. Also found that LPA3 was also highly expressed in ovarian cancer tissue and ovarian cancer cells. Importantly, LPA significantly promoted the proliferation and migration of LPA3-overexpressing ovarian cancer cells, while the LPA-induced actions blocked by Ki16425, a LPAR1/3 antagonist treated, and LPA3-shRNA transfected. In vivo study indicated that the LPA3-overexpressing cell derived tumors metastasis, tumors volume and tumors mass were apparently increased in xenografted nude mice. In addition, we also observed that LPA3 was differential high-expression in ovarian cancer tissue of the patients. Our studies further confirmed the LPA3/Gi/MAPKs/NF-κB signals were involved in LPA-induced oncogenic actions in ovarian cancer cells. Our findings indicated that the LPA3 might be a novel precise therapeutic target and potential biomarker for ovarian cancer.

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