scholarly journals Time-Dependent Effects of POT1 Knockdown on Proliferation, Tumorigenicity, and HDACi Response of SK-OV3 Ovarian Cancer Cells

2018 ◽  
Vol 2018 ◽  
pp. 1-12 ◽  
Author(s):  
Hua Zhou ◽  
Abdul Mondal ◽  
Aleksandra Dakic ◽  
Lama Alhawas ◽  
Xuefeng Liu ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Cell Proliferation ◽  
Telomerase Activity ◽  
Population Doubling ◽  
Ovarian Cancer Cells ◽  
Human Ovarian Cancer ◽  
Activity Levels ◽  
Mrna Levels ◽  
The Impact

The roles of protection of telomeres 1 (POT1) in human ovarian cancer have not been fully elucidated. Here, we investigated the impact of POT1 knockdown (POT1-KD) on in vitro cell proliferation, tumorigenesis, and histone deacetylase inhibitor (HDACi) response in human ovarian cancer-derived SK-OV3 cells. The POT1 gene was knocked down by infection with POT1 lenti-shRNA. POT1, c-Myc, and hTERT mRNA levels and relative telomere length were determined by qRT-PCR; POT1 protein levels were determined by western blot. The relative telomerase activity levels were detected using qTRAP; cell proliferation was assessed using cumulative population doubling (cPD) experiments. Cell tumorigenicity was evaluated by anchorage-independent cell growth assays, and cell response to HDACi was determined by luminescence cell viability assays. Results indicate that lenti-shRNA-mediated POT1-KD significantly reduced POT1 mRNA and protein expression. POT1-KD immediately downregulated c-Myc expression, which led to the inhibition of cell proliferation, tumorigenesis, and HDACi response. However, after brief suppression, c-Myc expression increased in the medium term, which resulted in enhanced cell proliferation, tumorigenesis, and HDACi response in the POT1-KD cells. Furthermore, we discovered that c-Myc regulated cell proliferation and tumorigenesis via hTERT/telomerase/telomere pathway.

scholarly journals Platelet-activating factor acetyl hydrolase IB2 dysregulated cell proliferation in ovarian cancer

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
YingYing He ◽  
Zhicheng He ◽  
Xiaoyu Zhang ◽  
Shubai Liu
Keyword(s):  
Ovarian Cancer ◽  
Cell Proliferation ◽  
Platelet Activating Factor ◽  
Regulatory Subunit ◽  
Ovarian Cancer Cells ◽  
Cancer Tissue ◽  
Serine Esterase ◽  
Cancer Pathogenesis ◽  
The Impact

Abstract Background Ovarian cancer is the leading cause of death from gynaecologic illnessed worldwide. Platelet-activating factor acetyl hydrolase IB2 (PAF-AH IB2) is an intracellular serine esterase that hydrolyzes platelet-activating factor, a G-protein-like trimer with two catalytic subunits and one regulatory subunit. The regulatory role of PAF-AH IB2 in the oncogenesis of ovarian cancer is not well understood. Methods In this study, the TCGA dataset and clinical cancer tissue microarray were utilized to investigate abnormal overexpression of PAF-AH IB2 in ovarian cancer. To investigate the impact on the cell proliferation, migration, and tumorigenicity in vitro, PAF-AH IB2 stable knocking down (KD) ovarian cancer cells were established by ShRNA. The whole transcription profiling, tyrosine kinase profiling and standard cell functional assays were integrated to explore the biological importance and mechanism of PAF-AH IB2 modulated in ovarian cancer. Results PAF-AH IB2 was identified significantly overexpression in four subtypes of ovarian cancer. In vitro, PAF-AH IB2 KD significantly inhibited cancer cell proliferation, migration, and tumorigenicity, activated caspases and caused cell cycle arrest, and made the cells more sensitive to PAF. PAF-AH 1B2 KD cells down-regulated several key regulators of the multiple tyrosine kinases-mediated signaling pathway, suggesting a novel interaction network between the growth factor receptors pathway and PAF-AH 1B2 mediated PAF signalling. Conclusions These findings revealed a previously undiscovered role for PAF-AH IB2 as a potenial therapy target and essential signaling mediators in ovarian cancer pathogenesis, as well as new possible preventive and therapeutic strategies to inhibit this enzyme in clinical treatment for ovarian cancer.

scholarly journals Platelet-activating Factor Acetyl Hydrolase IB2 Dysregulated Cell Proliferation in Ovarian Cancer

2021 ◽  
Author(s):  
yingying he ◽  
zhicheng he ◽  
Xiaoyu Zhang ◽  
SHUBAI LIU
Keyword(s):  
Ovarian Cancer ◽  
Cell Proliferation ◽  
Platelet Activating Factor ◽  
Regulatory Subunit ◽  
Ovarian Cancer Cells ◽  
Cancer Tissue ◽  
Serine Esterase ◽  
Cancer Pathogenesis ◽  
The Impact

Abstract BackgroundOvarian cancer is the world’s largest cause of death for gynaecologic diseases. Platelet-activating factor acetyl hydrolase IB2 (PAF-AH IB2) is an intracellular serine esterase that hydrolyzes platelet-activating factor, a G-protein-like trimer with two catalytic subunits and one regulatory subunit. The deregulatory role of PAF-AHIB2 in the etiology of ovarian cancer is poorly understood. MethodsIn this study, the TCGA exploration and cancer tissue immunohistochemistry were utilized to investigate aberrant overexpression of PAF-AH IB2 in ovarian cancer. PAF-AH IB2 Stable knocking down (KD) ovarian cancer cells were established to investigate the impact on the cell proliferation, migration, and tumorigenicity in vitro. The whole transcription profiling, tyrosine kinase profiling and standard cell functional assays were integrated to explore the biological importance and mechanism of PAF-AH IB2 modulated in ovarian cancer. ResultsInteresting, PAF-AH IB2 was identified significantly overexpression in four subtypes of ovarian cancer. PAF-AHIB2 KD significantly reduced cancer cell proliferation, migration, and tumorigenicity in vitro, activated Caspases and caused cell cycle arrest, and making the cells more sensitive to PAF. Several key regulators of multiple tyrosine kinases-mediated signaling pathway were down-regulated in PAF-AH 1B2 KD cells, revealing a novel interaction network between the growth factor receptors pathway and PAF-AH 1B2 mediated PAF signalling.Conclusions These results discovered an unrevealed role for PAFAH IB2 as a novel potential therapy target and essential signaling mediators in ovarian cancer pathogenesis, as well as new potential preventive and therapeutic strategies to inhibit this enzyme in clinical treatment for ovarian cancer.

scholarly journals Piperine Targets Different Drug Resistance Mechanisms in Human Ovarian Cancer Cell Lines Leading to Increased Sensitivity to Cytotoxic Drugs

2021 ◽  
Vol 22 (8) ◽  
pp. 4243
Author(s):  
Karolina Wojtowicz ◽  
Karolina Sterzyńska ◽  
Monika Świerczewska ◽  
Michał Nowicki ◽  
Maciej Zabel ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Cell Proliferation ◽  
Cell Lines ◽  
Cancer Cell ◽  
Cytotoxic Effect ◽  
Ovarian Cancer Cell ◽  
Ovarian Cancer Cells ◽  
Human Ovarian Cancer ◽  
Anticancer Effects ◽  
The Impact

Our goal was to examine the anticancer effects of piperine against the resistant human ovarian cancer cells and to explore the molecular mechanisms responsible for its anticancer effects. Our study used drug-sensitive ovarian cancer cell line W1 and its sublines resistant to paclitaxel (PAC) and topotecan (TOP). We analyzed the cytotoxic effect of piperine and cytostatic drugs using an MTT assay. The impact of piperine on protein expression was determined by immunofluorescence and Western blot. We also examined its effect on cell proliferation and migration. We noticed a different level of piperine resistance between cell lines. Piperine increases the cytotoxic effect of PAC and TOP in drug-resistant cells. We observed an increase in PTPRK expression correlated with decreased pTYR level after piperine treatment and downregulation of P-gp and BCRP expression. We also noted a decrease in COL3A1 and TGFBI expression in investigated cell lines and increased COL3A1 expression in media from W1PR2 cells. The expression of Ki67 protein and cell proliferation rate decreased after piperine treatment. Piperine markedly inhibited W1TR cell migration. Piperine can be considered a potential anticancer agent that can increase chemotherapy effectiveness in cancer patients.

scholarly journals E-cadherin promotes proliferation of human ovarian cancer cells in vitro via activating MEK/ERK pathway

2012 ◽  
Vol 33 (6) ◽  
pp. 817-822 ◽  
Author(s):  
Ling-ling Dong ◽  
Lian Liu ◽  
Chun-hong Ma ◽  
Ji-sheng Li ◽  
Chao Du ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Cancer Cells ◽  
Ovarian Cancer Cells ◽  
Human Ovarian Cancer ◽  
Erk Pathway ◽  
E Cadherin

scholarly journals STK3 Suppresses Ovarian Cancer Progression by Activating NF-κB Signaling to Recruit CD8+ T-Cells

2020 ◽  
Vol 2020 ◽  
pp. 1-17
Author(s):  
Xiangyu Wang ◽  
Fengmian Wang ◽  
Zhi-Gang Zhang ◽  
Xiao-Mei Yang ◽  
Rong Zhang ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Cell Proliferation ◽  
T Cells ◽  
Tumor Growth ◽  
Cd8 T Cells ◽  
Gene Set Enrichment Analysis ◽  
Ovarian Cancer Cells ◽  
And Migration

Serine/threonine protein kinase-3 (STK3) is a critical molecule of the Hippo pathway but little is known about its biological functions in the ovarian cancer development. We demonstrated the roles of STK3 in ovarian cancer. Existing databases were used to study the expression profile of STK3. STK3 was significantly downregulated in OC patients, and the low STK3 expression was correlated with a poor prognosis. In vitro cell proliferation, apoptosis, and migration assays, and in vivo subcutaneous xenograft tumor models were used to determine the roles of STK3. The overexpression of STK3 significantly inhibited cell proliferation, apoptosis, and migration of ovarian cancer cells in vitro and tumor growth in vivo. Bisulfite sequencing PCR analysis was performed to validate the methylation of STK3 in ovarian cancer. RNA sequencing and gene set enrichment analysis (GSEA) were used to compare the transcriptome changes in the STK3 overexpression ovarian cancer and control cells. The signaling pathway was analyzed by western blotting. STK3 promoted the migration of CD8+ T-cells by activating nuclear transcription factor κB (NF-κB) signaling. STK3 is a potential predictor of OC. It plays an important role in suppressing tumor growth of ovarian cancer and in chemotaxis of CD8+ T-cells.

scholarly journals Demethoxycurcumin inhibited human epithelia ovarian cancer cells’ growth via up-regulating miR-551a

Tumor Biology ◽  
2017 ◽  
Vol 39 (3) ◽  
pp. 101042831769430 ◽  
Author(s):  
Zhenhua Du ◽  
Xianqun Sha
Keyword(s):  
Ovarian Cancer ◽  
Cell Proliferation ◽  
Cancer Cells ◽  
Ovarian Cancer Cells ◽  
Natural Form ◽  
Ovarian Cancer Cell Lines ◽  
Induced Apoptosis ◽  
Tumor Suppressive Function ◽  
Cancer Tissues

Curcumin is a natural agent that has ability to dampen tumor cells’ growth. However, the natural form of curcumin is prone to degrade and unstable in vitro. Here, we demonstrated that demethoxycurcumin (a curcumin-related demethoxy compound) could inhibit cell proliferation and induce apoptosis of ovarian cancer cells. Moreover, IRS2/PI3K/Akt axis was inactivated in cells treated with demethoxycurcumin. Quantitative real-time reverse transcription polymerase chain reaction demonstrated that miR-551a was down-regulated in ovarian cancer tissues and ovarian cancer cell lines. Over-expression of miR-551a inhibited cell proliferation and induced apoptosis of ovarian cancer cells, whereas down-regulation of miR-551a exerted the opposite function. Luciferase assays confirmed that there was a binding site of miR-551a in IRS2, and we found that miR-551a exerted tumor-suppressive function by targeting IRS2 in ovarian cancer cells. Remarkably, miR-551a was up-regulated in the cells treated with demethoxycurcumin, and demethoxycurcumin suppressed IRS2 by restoration of miR-551a. In conclusion, demethoxycurcumin hindered ovarian cancer cells’ malignant progress via up-regulating miR-551a.

MiR-661 contributed to cell proliferation of human ovarian cancer cells by repressing INPP5J expression

2015 ◽  
Vol 75 ◽  
pp. 123-128 ◽  
Author(s):  
Tongyu Zhu ◽  
Jing Yuan ◽  
Yuzhi Wang ◽  
Cuiping Gong ◽  
Yudou Xie ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Cell Proliferation ◽  
Cancer Cells ◽  
Ovarian Cancer Cells ◽  
Human Ovarian Cancer

Heterogeneous interaction of interferon-β and taxol in human ovarian cancer cells in vitro

1994 ◽  
Vol 30 (6) ◽  
pp. 892-893
Author(s):  
S. Sen ◽  
A. Zocchetti ◽  
P. Beccaglia ◽  
G. Balconi ◽  
E. Erba ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Cancer Cells ◽  
Ovarian Cancer Cells ◽  
Human Ovarian Cancer ◽  
Interferon Β ◽  
Heterogeneous Interaction
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