scholarly journals Effect of Ginsenoside Rh-2 via Activation of Caspase-3 and Bcl-2-Insensitive Pathway in Ovarian Cancer Cells

2016 ◽  
pp. 1031-1037 ◽  
Author(s):  
J. H. KIM ◽  
J.-S. CHOI
Keyword(s):  
Ovarian Cancer ◽  
Cell Proliferation ◽  
Cancer Cells ◽  
Caspase 3 ◽  
Therapeutic Potential ◽  
Future Application ◽  
Ovarian Cancer Cells ◽  
Therapeutic Effects ◽  
Apoptosis Pathway ◽  
Skov3 Cells

Ginsenoside has been reported to have therapeutic effects for some types of cancer, but its effect on ovarian cancer cells has not been evaluated. In this study, we monitored the effects of ginsenoside-Rh2 (Rh2) on the inhibition of cell proliferation and the apoptotic process in the ovarian cancer cell line SKOV3 using an MTT assay and TUNEL assay. We found that Rh2 inhibited cell proliferation and significantly induced apoptosis. We confirmed the apoptotic effects of Rh2 using western blot analysis of apoptosis-related proteins. Specifically, the levels of cleaved poly ADP ribose polymerase (PARP) and cleaved caspase-3 significantly increased in SKOV3 cells treated with Rh2. Therefore, Rh2 clearly suppressed the growth of SKOV3 cells in vitro, which was associated with induction of the apoptosis pathway. Moreover, the migration assay showed that Rh2 inhibited the invasive ability of SKOV3 cells. Taken together, our results suggest that Rh2 has anticancer effects in SKOV3 cells through inhibition of cell proliferation and induction of apoptosis. Considering the therapeutic potential of Rh2, more studies should be carried out to facilitate the future application of this natural product as a potential anti-cancer agent.

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.

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.

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 Membranous and Cytoplasmic Expression of PD-L1 in Ovarian Cancer Cells

2017 ◽  
Vol 43 (5) ◽  
pp. 1893-1906 ◽  
Author(s):  
Qiu-Xia Qu ◽  
Fang Xie ◽  
Qin Huang ◽  
Xue-Guang Zhang
Keyword(s):  
Ovarian Cancer ◽  
Cancer Cells ◽  
Immune Evasion ◽  
Cell Function ◽  
Therapeutic Potential ◽  
Pi3k Pathway ◽  
Ovarian Cancer Cells ◽  
Tumor Growth Inhibition ◽  
Skov3 Cells

Background: Expression of programmed death-ligand 1 (PD-L1) on tumor cells represents a powerful immune evasion pathway, but the role of intracellular or cytoplasmic PD-L1 has not been investigated in ovarian cancer cells. Methods: Flow cytometry (FCM), Real-time PCR (qPCR), immunohistochemistry (IHC) and western blot were used to determine the expression of PD-L1 in ovarian cancer cells. The cytokines detected in the tumor or tumor associated macrophage (TAM) were used to treat cancer cells. PD-L1 blockade and silencing were used to elucidate the functional significance of cancer-related PD-L1 expression. Results: Based on the results presented, PD-L1 was found variably expressed in the cytoplasm and the cell surface of both HO8910 and SKOV3 cells. TAM or IFN-γ, TNF-α, IL-10 and IL-6 released from TAM stimulated the expression of PD-L1 at the surface of the cancer cells. The IHC results were consistent with the data in vitro showing infiltration of TAM correlated with membranous PD-L1. The increases of PD-L1 at the surface were not due to a shift in the proportion of surface versus intracellular protein, but the contribution of extracellular signal-regulated kinase (ERK)1/2 and phosphoinositide 3-kinase (PI3K) pathway activation. As a consequence, inducible membranous PD-L1 expression on SKOV3 inhibited CD8+ T cell function, and cytoplasmic PD-L1 promoted cancer cell growth. Additionally, in mouse models, both PD-L1 and PD-1 mAb resulted in tumor growth inhibition and demonstrated a potential to decrease the number of PD-1+CD8+T cells. Conclusion: We conclude that TAM induced PD-L1 on the cancer cells represents an immune evasion mechanism. The observations confirm the therapeutic potential of PD-L1/PD-1 mAb to reactivate anti-tumor immunity in ovarian cancer.

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.

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 ovarian cancer 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, the mechanism study showed that dezocine could significantly inhibit the expression of CRABP2, and CRABP2 overexpression reversed the inhibitory effects of dezocine on ovarian cancer cell proliferation and migration. Conclusions: 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 Electrochemotherapy with Calcium Chloride and 17β-Estradiol Modulated Viability and Apoptosis Pathway in Human Ovarian Cancer

Pharmaceutics ◽  
2020 ◽  
Vol 13 (1) ◽  
pp. 19
Author(s):  
Zofia Łapińska ◽  
Michał Dębiński ◽  
Anna Szewczyk ◽  
Anna Choromańska ◽  
Julita Kulbacka ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Cancer Cells ◽  
Calcium Chloride ◽  
Morphological Changes ◽  
Cell Membrane Permeability ◽  
Immunocytochemical Staining ◽  
Ovarian Cancer Cells ◽  
Apoptosis Pathway ◽  
17Β Estradiol

Estrogens (Es) play a significant role in the carcinogenesis and progression of ovarian malignancies. Depending on the concentration, Es may have a protective or toxic effect on cells. Moreover, they can directly or indirectly affect the activity of membrane ion channels. In the presented study, we investigated in vitro the effectiveness of the ovarian cancer cells (MDAH-2774) pre-incubation with 17β-estradiol (E2; 10 µM) in the conventional chemotherapy (CT) and electrochemotherapy (ECT) with cisplatin or calcium chloride. We used three different protocols of electroporation including microseconds (µsEP) and nanoseconds (nsEP) range. The cytotoxic effect of the applied treatment was examined by the MTT assay. We used fluorescent staining and holotomographic imaging to observe morphological changes. The immunocytochemical staining evaluated the expression of the caspase-12. The electroporation process’s effectiveness was analyzed by a flow cytometer using the Yo-Pro™-1 dye absorption assay. We found that pre-incubation of ovarian cancer cells with 17β-estradiol may effectively enhance the chemo- and electrochemotherapy with cisplatin and calcium chloride. At the same time, estradiol reduced the effectiveness of electroporation, which may indicate that the mechanism of increasing the effectiveness of ECT by E2 is not related to the change of cell membrane permeability.

scholarly journals PML silencing inhibits cell proliferation and induces DNA damage in cultured ovarian cancer cells

2017 ◽  
Vol 7 (1) ◽  
pp. 29-35 ◽  
Author(s):  
Sheng-Bing Liu ◽  
Zhong-Fei Shen ◽  
Yan-Jun Guo ◽  
Li-Xian Cao ◽  
Ying Xu
Keyword(s):  
Ovarian Cancer ◽  
Cell Proliferation ◽  
Dna Damage ◽  
Cancer Cells ◽  
Ovarian Cancer Cells

scholarly journals Dasatinib (BMS-35482) Interacts Synergistically With Docetaxel, Gemcitabine, Topotecan, and Doxorubicin in Ovarian Cancer Cells With High SRC Pathway Activation and Protein Expression

2014 ◽  
Vol 24 (2) ◽  
pp. 218-225 ◽  
Author(s):  
Angeles Alvarez Secord ◽  
Deanna Teoh ◽  
Jingquan Jia ◽  
Andrew B. Nixon ◽  
Lisa Grace ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Protein Expression ◽  
Cancer Cells ◽  
Combination Index ◽  
Chemotherapeutic Agents ◽  
Cytotoxic Agents ◽  
Ovarian Cancer Cells ◽  
Response Curves ◽  
Pathway Activation ◽  
Skov3 Cells

PurposeThis study aimed to explore the activity of dasatinib in combination with docetaxel, gemcitabine, topotecan, and doxorubicin in ovarian cancer cells.MethodsCells with previously determined SRC pathway and protein expression (SRC pathway/SRC protein IGROV1, both high; SKOV3, both low) were treated with dasatinib in combination with the cytotoxic agents. SRC and paxillin protein expression were determined pretreatment and posttreatment. Dose-response curves were constructed, and the combination index (CI) for drug interaction was calculated.ResultsIn the IGROV1 cells, dasatinib alone reduced phospho-SRC/total SRC 71% and p-paxillin/t-paxillin ratios 77%. Phospho-SRC (3%–33%; P = 0.002 to 0.04) and p-paxicillin (6%–19%; P = 0.01 to 0.05) levels were significantly reduced with dasatinib in combination with each cytotoxic agent. The combination of dasatinib and docetaxel, gemcitabine, or topotecan had a synergistic antiproliferative effect (CI, 0.49–0.68), whereas dasatinib combined with doxorubicin had an additive effect (CI, 1.08).In SKOV3 cells, dasatinib resulted in less pronounced reductions of phospho-SRC/total SRC (49%) and p-paxillin/t-paxillin (62%). Phospho-SRC (18%; P < 0.001) and p-paxillin levels (18%; P = 0.001; 9%; P = 0.007) were significantly decreased when dasatinib was combined with docetaxel and topotecan (p-paxillin only). Furthermore, dasatinib combined with the cytotoxics in the SKOV3 cells produced an antagonistic interaction on the proliferation of these cells (CI, 1.49–2.27).ConclusionsDasatinib in combination with relapse chemotherapeutic agents seems to interact in a synergistic or additive manner in cells with high SRC pathway activation and protein expression. Further evaluation of dasatinib in combination with chemotherapy in ovarian cancer animal models and exploration of the use of biomarkers to direct therapy are warranted.

Sign in / Sign up

Export Citation Format

Share Document