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 ◽  
...  

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.

RSC Advances ◽  
2019 ◽  
Vol 9 (45) ◽  
pp. 25957-25966
Author(s):  
Gökçen Yaşayan ◽  
Oya Orun ◽  
Pınar Mega Tiber ◽  
Veronika Rožman ◽  
Sevgi Koçyiğit Sevinç

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


2020 ◽  
Author(s):  
Chun Hua Liu ◽  
Xue Ning Jing ◽  
Xiao Lan Liu ◽  
Shan Yong Qin ◽  
Min Wei Liu ◽  
...  

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.


2020 ◽  
Vol 12 (3) ◽  
pp. 361-367
Author(s):  
Xiaoping Chen ◽  
Xinping Ren ◽  
Jinling Xue ◽  
Ling Xi

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.


2007 ◽  
Vol 406 (3) ◽  
pp. 427-436 ◽  
Author(s):  
Yuanda Song ◽  
Palmer Wilkins ◽  
Wenhui Hu ◽  
Karnam S. Murthy ◽  
Jing Chen ◽  
...  

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.


2021 ◽  
Vol 11 (3) ◽  
pp. 407-411
Author(s):  
Shenhua Zhang ◽  
Ting Yu

We investigated the effects of silencing the regulator of ribosome synthesis 1 (RRS1) gene on the proliferation, migration, and invasion of ovarian carcinoma cells, and its possible role in modulating signal transduction in these cells. Normal ovarian epithelial cell line IOSE80 was used as a control. We examined the mRNA and protein level of RRS1 using qRT-PCR and western blot in control and ovarian carcinoma cells (SKOV-3, SW626, and CAOV3). RNA interference technology was used to knockdown RRS1 expression in CAOV3 cells. MTT was used to examine the proliferation of these cells, while a Transwell assay was used to assay the cells’ migration and invasion abilities. Western blot was used to measure the levels of CyclinD1, P21, MMP-2, MMP-9, p-JAK2 and p-STAT3 proteins. In comparison with normal ovarian epithelial cells (IOSE80), RRS1 mRNA and protein levels were increased in ovarian carcinoma cells (SKOV-3, SW626 and CAOV3) (P < 0.05). Because RRS1 levels were highest in CAOV3 cells, these cells were used for subsequent experiments. RRS1 gene expression was knocked down in CAOV3 cells, and in comparison with the negative control group, siRNA-RRS1 cells exhibited decreased proliferation in the MTT assay after 48 h and 72 h (P < 0.05). These cells also exhibited reduced migration and invasion (P < 0.05). Further, siRNA-RRS1 cells exhibited reduced expression of CyclinD1, MMP-2, MMP-9, P-JAK2 and P-STAT3 proteins (P < 0.05), while P21 protein levels were increased (P < 0.05). Silencing RRS1 expression inhibits the proliferation, migration, and invasion of ovarian carcinoma cells. This effect may be mediated by the inhibition of the STAT3 signaling pathway in these cells.


2020 ◽  
Vol 44 (35) ◽  
pp. 14928-14935
Author(s):  
Carolina G. Oliveira ◽  
Luciana F. Dalmolin ◽  
R. T. C. Silva ◽  
Renata F. V. Lopez ◽  
Pedro I. S. Maia ◽  
...  

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).


2017 ◽  
Vol 88 (6) ◽  
pp. 307-311
Author(s):  
Jacek Sieńko ◽  
Witold Lasek ◽  
Justyna Teliga-Czajkowska ◽  
Roman Smolarczyk ◽  
Krzysztof Czajkowski

Molecules ◽  
2019 ◽  
Vol 24 (4) ◽  
pp. 673 ◽  
Author(s):  
Ying Gao ◽  
Junfeng Yin ◽  
Youying Tu ◽  
Yi Chen

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.


2006 ◽  
Vol 1 ◽  
pp. 117727190600100 ◽  
Author(s):  
Akiko Horiuchi ◽  
Cuiju Wang ◽  
Norihiko Kikuchi ◽  
Ryosuke Osada ◽  
Toshio Nikaido ◽  
...  

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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