scholarly journals Assessment of Antitumor Activity of Vinca herbacea on Human Ovarian Cancer Cell Line

2021 ◽  
Vol 3 (2) ◽  
pp. 115-126
Author(s):  
Somayeh Dehghanipour ◽  
◽  
Sara Saadatmand ◽  
Nasim Hayati Roodbari ◽  
Mehdi Mahdavi ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Ovarian Cancer Cell Line ◽  
Ovarian Cancer Cells ◽  
Human Ovarian Cancer ◽  
Dependent Manner ◽  
Matrigel Invasion Assay ◽  
Matrigel Invasion ◽  
Skov3 Cells

Background: It seems that Vinca. herbacea has an anti-tumor effect. Here, the immunotherapeutic effect of this compound is assessed against human ovarian cancer (SKOV3) cells because of the high incidence of this tumor in women. Materials and Methods: The cytotoxic activity of V. herbacea extract against human ovarian cancer (SKOV3) cells was determined by MTT assay. The apoptosis-inducing potential of V. herbacea extract was investigated using the FITC-V Annexin kit. The Matrigel invasion assay was used to investigate the ability of V. herbacea extract in reducing ovarian cancer cells invasion. Real-time PCR using specific primers was performed to investigate the expression of angiogenesis (VEGFR1, VEGFR2, and VEGF-A), apoptosis (Bcl-2 and Bax), and metastasis (MMP2 and MMP9) genes. Results: V. herbacea caused a significant cytotoxic effect against human ovarian cancer cells in a dose-dependent manner. V. herbacea induced apoptosis in SKOV3 cells through caspase-3 activation and an increase in the expression ratio of Bax/Bcl-2. V. herbacea inhibited cancer cells’ angiogenesis, which was evident by the significant reduction in the expression of angiogenesis-related genes, including VEGF, VEGFR-1, and VEGFR-2. Besides, V. herbacea inhibited cancer cell adhesion and invasion. Conclusion: V. herbacea extract elicits a robust cytostatic effect in SKOV3 cells by modulating the activity and or the expression of proteins regulating the process of cellular apoptosis, adhesion invasion, and angiogenesis.

scholarly journals Proapoptotic Protein Smac Mediates Apoptosis in Ovarian Cancer Cells When ‎Treated with the Carpachromene ‎

2021 ◽  
Author(s):  
Yunjing Song ◽  
Jian Wang ◽  
Chunnian Zhang ◽  
Ying Yu ◽  
Hong Cai
Keyword(s):  
Ovarian Cancer ◽  
Cancer Cells ◽  
Cell Line ◽  
Cancer Cell ◽  
Ovarian Cancer Cell ◽  
Ovarian Cancer Cell Line ◽  
Cancer Cell Line ◽  
Ovarian Cancer Cells ◽  
Human Ovarian Cancer ◽  
Human Ovarian Cancer Cell

IntroductionWe also investigated the Carpachromene in the cytotoxicity studies against common human ovarian cancer cell ‎line i.e., SW 626, in-vitro.Material and methodsCell viability of Carpachromene was very low against common ‎human ovarian cancer ‎cell line i.e. SW 626 without any cytotoxicity on normal cell line. To compare the ‎biological activities of molecules, the enzymes used are α-glucosidase, acetylcholinesterase, respectively. Finally, ‎calculations were made using the molecular docking method to compare the biological activity of the ‎carpachromene molecule. We then examined whether the release of Smac is necessary for apoptosis in ovarian ‎cancer cells using the SW 626‎ cell line. We first examined mitochondrial and cytosolic Smac levels after ‎Carpachromene treatment. ‎ResultsFollowing the docking calculations, the properties of the carpachromene molecule ‎were examined by ADME/T analysis in order to be used as a drug in the future. In addition, the anti-oxidant ‎properties of the molecules were examined in both gas and water phase with the HF/6-31g basis set with the ‎Gaussian software program. As shown, exposure of ovarian cancer cells to Carpachromene decreased ‎mitochondrial Smac and increased cytosolic Smac levels in a time-dependent fashion. As depicted in results, a ‎decrease in Smac expression was confirmed by Western blot. Silencing of Smac significantly inhibited ‎Carpachromene-induced caspase-3 cleavage and attenuated apoptosis in these cells Moreover, overexpression of ‎a Smac heptapeptide (Smac-N7) enhanced Carpachromene-induced cell deathConclusionsAccording to the above findings, the Carpachromene may be administrated for the treatment of several types of ‎human ovarian cancer in humans. ‎

scholarly journals CC Chemokine Ligand 7 Derived from Cancer-Stimulated Macrophages Promotes Ovarian Cancer Cell Invasion

Cancers ◽  
2021 ◽  
Vol 13 (11) ◽  
pp. 2745
Author(s):  
Miran Jeong ◽  
Yi-Yue Wang ◽  
Ju-Yeon Choi ◽  
Myong-Cheol Lim ◽  
Jung-Hye Choi
Keyword(s):  
Ovarian Cancer ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Cell Invasion ◽  
Ovarian Cancer Cell ◽  
Ovarian Cancer Cells ◽  
Human Ovarian Cancer ◽  
Cancer Cell Invasion ◽  
Cc Chemokine ◽  
Chemokine Ligand

In the tumor microenvironment, macrophages have been suggested to be stimulated by tumor cells, becoming tumor-associated macrophages that promote cancer development and progression. We examined the effect of these macrophages on human ovarian cancer cell invasion and found that conditioned medium of macrophages stimulated by ovarian cancer cells (OC-MQs) significantly increased cell invasion. CC chemokine ligand 7 (CCL7) expression and production were significantly higher in OC-MQs than in the control macrophages. Peritoneal macrophages from patients with ovarian cancer showed higher CCL7 expression levels than those from healthy controls. Inhibition of CCL7 using siRNA and neutralizing antibodies reduced the OC-MQ-CM-induced ovarian cancer cell invasion. CC chemokine receptor 3 (CCR3) was highly expressed in human ovarian cancer cells, and a specific inhibitor of this receptor reduced the OC-MQ-CM-induced invasion. Specific signaling and transcription factors were associated with enhanced CCL7 expression in OC-MQs. CCL7-induced invasion required the expression of matrix metalloproteinase 9 via activation of extracellular signal-related kinase signaling in human ovarian cancer cells. These data suggest that tumor-associated macrophages can affect human ovarian cancer metastasis via the CCL7/CCR3 axis.

scholarly journals LHRH might act as a negative autocrine regulator of proliferation of human ovarian cancer

2000 ◽  
pp. 665-670 ◽  
Author(s):  
G Emons ◽  
S Weiss ◽  
O Ortmann ◽  
C Grundker ◽  
KD Schulz
Keyword(s):  
Ovarian Cancer ◽  
Cancer Cells ◽  
Cell Lines ◽  
Cancer Cell ◽  
Ovarian Cancer Cell ◽  
Ovarian Cancer Cells ◽  
Human Ovarian Cancer ◽  
Lhrh Agonists ◽  
Ovarian Cancer Cell Lines ◽  
Low Concentrations

OBJECTIVE: More than 80% of human ovarian cancers express LHRH and its receptor. The proliferation of human ovarian cancer cell lines is reduced by both LHRH agonists and antagonists. This study was designed to further clarify the possible biological function of this LHRH system. DESIGN: As LHRH agonists and antagonists uniformly reduce proliferation of human ovarian cancer in a dose-dependent way, the effect of low concentrations of authentic LHRH was studied. In addition, longer periods of treatment (up to 9 days) were analyzed. To assess the physiological role of LHRH produced by ovarian cancer cells it was neutralized by adequate concentrations of a specific LHRH antiserum. METHODS: Human ovarian cancer cells EFO-21 and EFO-27, which express LHRH and its receptor, were incubated for 1-9 days with increasing concentrations (1pmol/l to 10 micromol/l) of authentic LHRH or with concentrations of LHRH antiserum capable of neutralizing at least 1nmol/l LHRH. Proliferation was assessed by counting cells. RESULTS AND CONCLUSIONS: Authentic LHRH reduced time- and dose-dependently proliferation (by maximally mean+/-s.e.m. 32.7 +/- 4.4%, Newman-Keuls, P < 0.001) of both ovarian cancer cell lines. At very low concentrations (1pmol/l) a marginal reduction of proliferation or no effect was observed. A mitogenic effect of authentic LHRH was never detected. Treatment of ovarian cancer cell cultures with antiserum to LHRH significantly increased (up to mean+/-s.e.m. 121.0 +/- 2.8% of controls, Newman-Keuls P <0.001) proliferation of EFO-21 and EFO-27 cells. These findings suggest that LHRH produced by human ovarian cancer cells might act as a negative autocrine regulator of proliferation.

scholarly journals Clerodane Diterpenoids from an Edible Plant Justicia insularis: Discovery, Cytotoxicity, and Apoptosis Induction in Human Ovarian Cancer Cells

Molecules ◽  
2021 ◽  
Vol 26 (19) ◽  
pp. 5933
Author(s):  
Idowu E. Fadayomi ◽  
Okiemute R. Johnson-Ajinwo ◽  
Elisabete Pires ◽  
James McCullagh ◽  
Tim D. W. Claridge ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Cancer Cells ◽  
Caspase 3 ◽  
Ovarian Cancer Cells ◽  
Human Ovarian Cancer ◽  
Dependent Manner ◽  
Edible Plant ◽  
Cytotoxic Compounds ◽  
Clerodane Diterpenoids ◽  
Induction Of Apoptosis

Objectives: The toxicity of chemotherapeutic anticancer drugs is a serious issue in clinics. Drug discovery from edible and medicinal plants represents a promising approach towards finding safer anticancer therapeutics. Justicia insularis T. Anderson (Acanthaceae) is an edible and medicinal plant in Nigeria. This study aims to discover cytotoxic compounds from this rarely explored J. insularis and investigate their underlying mechanism of action. Methods: The cytotoxicity of the plant extract was evaluated in human ovarian cancer cell lines and normal human ovarian surface epithelia (HOE) cells using a sulforhodamine B assay. Bioassay-guided isolation was carried out using column chromatography including HPLC, and the isolated natural products were characterized using GC-MS, LC-HRMS, and 1D/2D NMR techniques. Induction of apoptosis was evaluated using Caspase 3/7, 8, and 9, and Annexin V and PI based flow cytometry assays. SwissADME and SwissTargetPrediction web tools were used to predict the molecular properties and possible protein targets of identified active compounds. Key finding: The two cytotoxic compounds were identified as clerodane diterpenoids: 16(α/β)-hydroxy-cleroda-3,13(14)Z-dien-15,16-olide (1) and 16-oxo-cleroda-3,13(14)E-dien-15-oic acid (2) from the Acanthaceous plant for the first time. Compound 1 was a very abundant compound (0.7% per dry weight of plant material) and was shown to be more potent than compound 2 with IC50 values in the micromolar range against OVCAR-4 and OVCAR-8 cancer cells. Compounds 1 and 2 were less cytotoxic to HOE cell line. Both compounds induced apoptosis by increasing caspase 3/7 activities in a concentration dependent manner. Compound 1 further increased caspase 8 and 9 activities and apoptosis cell populations. Compounds 1 and 2 are both drug like, and compound 1 may target various proteins including a kinase. Conclusions: Clerodane diterpenoids (1 and 2) in J. insularis were identified as cytotoxic to ovarian cancer cells via the induction of apoptosis, providing an abundant and valuable source of hit compounds for the treatment of ovarian cancer.

scholarly journals Induction of mitochondria mediated apoptosis in human ovarian cancer cells by folic acid coated tin oxide nanoparticles

PLoS ONE ◽  
2021 ◽  
Vol 16 (10) ◽  
pp. e0258115
Author(s):  
Demiana H. Hanna ◽  
Gamal R. Saad
Keyword(s):  
Ovarian Cancer ◽  
Cancer Cells ◽  
Tin Oxide ◽  
Reactive Oxygen Species Generation ◽  
Ovarian Cancer Cells ◽  
Oxide Nanoparticles ◽  
Human Ovarian Cancer ◽  
Oxygen Species ◽  
Skov3 Cells ◽  
Tin Oxide Nanoparticles

Purpose This study aims to prepare folic acid coated tin oxide nanoparticles (FA-SnO2 NPs) for specifically targeting human ovarian cancer cells with minimum side effects against normal cells. Methods The prepared FA-SnO2 NPs were characterized by FT-IR, UV-vis spectroscopy, XRD, SEM and TEM. The inhibition effects of FA-SnO2 NPs against SKOV3 cancer cell were tested by MTT and LDH assay. Apoptosis induction in FA-SnO2 NPs treated SKOV3 cells were investigated using Annexin V/PI, AO/EB and Comet assays and the possible mechanisms of the cytotoxic action were studied by Flow cytometry, qRT-PCR, Immunohistochemistry, and Western blotting analyses. The effects of FA-SnO2 NPs on reactive oxygen species generation in SKOV3 cells were also examined. Additionally, the safety of utilization FA-SnO2 NPs were studied in vivo using Wister rats. Results The obtained FA-SnO2 NPs displayed amorphous spherical morphology with an average diameter of 157 nm and a zeta potential value of -24 mV. Comparing to uncoated SnO2 NPs, FA-SnO2 NPs had a superior inhibition effect towards SKOV3 cell growth that was suggested to be mediated through higher reactive oxygen species generation. It was showed that FA-SnO2 NPs increased significantly the % of apoptotic cells in the sub- G1 and G2/M phases with a higher intensity comet nucleus in SKOV3 treated cells. Furthermore, FA-SnO2 NPs was significantly increased the expression levels of P53, Bax, and cleaved Caspase-3 and accompanied with a significant decrease of Bcl-2 in the treated SKOV3 cells. Conclusion Overall, the results suggested that an increase in cellular FA-SnO2 NPs internalization resulted in a significant induced cytotoxicity in SKOV3 cancer cells in dose-dependent mode through ROS-mediated cell apoptosis that may have occurred through mitochondrial pathway. Additionally, the results confirmed the safety of utilization FA-SnO2 NPs against living systems. So, FA-SnO2 NPs with a specific targeting moiety may be a promising therapeutic candidate for human ovarian cancer.

scholarly journals UBE2S promotes the progression and Olaparib resistance of ovarian cancer through Wnt/β-catenin signaling pathway

2021 ◽  
Vol 14 (1) ◽  
Author(s):  
Wenjing Hu ◽  
Min Li ◽  
Youguo Chen ◽  
Xinxian Gu
Keyword(s):  
Ovarian Cancer ◽  
Cancer Cells ◽  
Signaling Pathway ◽  
Xenograft Model ◽  
Migration And Invasion ◽  
Ovarian Cancer Cells ◽  
Dependent Manner ◽  
Cancer Proliferation ◽  
Skov3 Cells

Abstract Background Ovarian cancer is the most lethal gynecologic malignancy worldwide. Olaparib, an inhibitor of poly (ADP-ribose) polymerase (PARP), is becoming widely used in ovarian cancer treatment. The overall survival of ovarian cancer has not been significantly changed over the past decades and ovarian cancer has become increasingly resistant to the Olaparib. Ubiquitin-conjugating enzyme E2S (UBE2S) has been proved to promote malignant behaviors in many cancers. However, the function of UBE2S in the development and Olaparib resistance of ovarian cancer are unclear. Materials and methods In this study, we detected the expression of UBE2S in normal fallopian tube (FT) and HGSOC tissues. A2780 and SKOV3 cells were stably transfected with PCMV-UBE2S, PCMV-UBE2S-C95S, UBE2S shRNAs, and negative controls. The CCK8 assay and clonogenic assay were conducted to analyze ovarian cancer proliferation and Olaparib resistance. The transwell assay was performed to determine the migration and invasion of ovarian cancer cells. The relative protein levels of the Wnt/β-catenin signaling pathway were tested using western blot. The ovarian cancer cells were treated with XAV-939 to investigate the role of Wnt/β-catenin signaling pathway in Olaparib resistance. Moreover, we repeated some above procedures in the xenograft model. Results The results demonstrated that UBE2S was highly upregulated in HGSOC and that high UBE2S expression was correlated with poor outcomes in HGSOC. UBE2S promoted ovarian cancer proliferation and drived the migration and invasion of ovarian cancer cells. UBE2S activated the Wnt/β-catenin signaling pathway in ovarian cancer resulting in Olaparib resistance in vitro and in vivo. Furthermore, UBE2S enhanced the proliferation and Olaparib resistance of ovarian cancer in its enzymatic activity dependent manner. Conclusions These data suggest a possible molecular mechanism of proliferation and metastasis of ovarian cancer and highlight the potential role of UBE2S as a therapeutic target in ovarian cancer.

Effects of nano-taxol/curcumin on ovarian cancer cells

2020 ◽  
Vol 10 (10) ◽  
pp. 1615-1619
Author(s):  
Shuai Zhang ◽  
Junhui Liang ◽  
Changzhong Li ◽  
Fei Wang
Keyword(s):  
Ovarian Cancer ◽  
Cell Proliferation ◽  
Cancer Cells ◽  
Culture Medium ◽  
Morphological Characteristics ◽  
Ovarian Cancer Cells ◽  
Human Ovarian Cancer ◽  
Pharmacodynamic Effect ◽  
Skov3 Cells ◽  
Inhibit Cell Proliferation

To investigate the pharmacodynamic effect of urushin nanoparticles upon the proliferation inhibition in human ovarian cancer SKOV3 cells, and in order to explore their biomechanism, the cell cycle and the percentage of apoptotic cells in human ovarian cancer SKOV3 cells were analyzed utilizing flow cytometry. The concentration of astragalin nanoparticles in SKOV3 cells was identified utilizing HPIC. Consequently, the morphological characteristics of SKOV3 cells in a culture medium of 5 mg/L were investigated and measured. In our findings, the 50 mg cancer cells containing 50 mg IC did not display this noted effect. The results exhibit the discovery that urushin nanoparticles inhibit cell proliferation, which is related to the inhibition of DNA replication and the regulation of the cell proliferation cycle. HPLC results demonstrated that the pharmacological effect of urushin nanoparticles was directly related to the drug concentration present within the studied cells. Hence, urushin nanoparticles can effectively enter cells and then effectively inhibit cell proliferation.

scholarly journals Inhibition of Ovarian Cancer Cell Spheroid Formation by Synthetic Peptides Derived from Nectin-4

2020 ◽  
Vol 21 (13) ◽  
pp. 4637
Author(s):  
Kristin L.M. Boylan ◽  
Rory D. Manion ◽  
Heena Shah ◽  
Keith M. Skubitz ◽  
Amy P. N. Skubitz
Keyword(s):  
Ovarian Cancer ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Synthetic Peptides ◽  
Ovarian Cancer Cell ◽  
Single Cells ◽  
Ovarian Cancer Cells ◽  
Dependent Manner ◽  
Spheroid Formation ◽  
Multicellular Spheroids

The formation of 3D multicellular spheroids in the ascites fluid of ovarian cancer patients is an understudied component of the disease progression. Spheroids are less sensitive to chemotherapy, in part due to the protection afforded by their structure, but also due to their slower proliferation rate. Previous studies suggest that the cell adhesion molecule Nectin-4 plays a key role in the formation of ovarian cancer spheroids. In this study, we further examined the role of Nectin-4 at early time points in spheroid formation using real-time digital photography. Human NIH:OVCAR5 ovarian cancer cells formed aggregates within 8 h, which further contracted into compact spheroids over 24 h. In contrast, Nectin-4 knockdown cells did not form tightly compacted spheroids. Synthetic peptides derived from Nectin-4 were tested for their ability to alter spheroid formation in two ovarian cancer cell lines. Nectin-4 peptide 10 (N4-P10) had an immediate effect on disrupting ovarian cancer spheroid formation, which continued for over 24 h, while a scrambled version of the peptide had no effect. N4-P10 inhibited spheroid formation in a concentration-dependent manner and was not cytotoxic; suggesting that N4-P10 treatment could maintain the cancer cells as single cells which may be more sensitive to chemotherapy.

scholarly journals Piperlongumine Induces Apoptosis and Synergizes with Cisplatin or Paclitaxel in Human Ovarian Cancer Cells

2014 ◽  
Vol 2014 ◽  
pp. 1-10 ◽  
Author(s):  
Li-Hua Gong ◽  
Xiu-Xiu Chen ◽  
Huan Wang ◽  
Qi-Wei Jiang ◽  
Shi-Shi Pan ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Cancer Cells ◽  
Cell Apoptosis ◽  
Therapeutic Potential ◽  
Ovarian Cancer Cells ◽  
Human Ovarian Cancer ◽  
Dependent Manner ◽  
Ros Accumulation ◽  
M Phase ◽  
Natural Alkaloid

Piperlongumine (PL), a natural alkaloid fromPiper longum L., possesses the highly selective and effective anticancer property. However, the effect of PL on ovarian cancer cells is still unknown. In this study, we firstly demonstrate that PL selectively inhibited cell growth of human ovarian cancer cells. Furthermore, PL notably induced cell apoptosis, G2/M phase arrest, and accumulation of the intracellular reactive oxidative species (ROS) in a dose- and time-dependent manner. Pretreatment with antioxidant N-acety-L-cysteine could totally reverse the PL-induced ROS accumulation and cell apoptosis. In addition, low dose of PL/cisplatin or paclitaxel combination therapies had a synergistic antigrowth effect on human ovarian cancer cells. Collectively, our study provides new therapeutic potential of PL on human ovarian cancer.

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