scholarly journals Identification of PARP-7 substrates reveals a role for MARylation in microtubule control in ovarian cancer cells

eLife ◽  
2021 ◽  
Vol 10 ◽  
Author(s):  
Lavanya H Palavalli Parsons ◽  
Sridevi Challa ◽  
Bryan A Gibson ◽  
Tulip Nandu ◽  
MiKayla S Stokes ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Cell Adhesion ◽  
Cancer Cells ◽  
Biological Activities ◽  
Global Gene Expression ◽  
Cytoskeletal Proteins ◽  
Ovarian Cancer Cells ◽  
Mrna Levels ◽  
Cancer Cell Growth ◽  
Cell Cell

PARP-7 (TiPARP) is a mono(ADP-ribosyl) transferase whose protein substrates and biological activities are poorly understood. We observed that PARP7 mRNA levels are lower in ovarian cancer patient samples compared to non-cancerous tissue, but PARP-7 protein nonetheless contributes to several cancer-related biological endpoints in ovarian cancer cells (e.g. growth, migration). Global gene expression analyses in ovarian cancer cells subjected to PARP-7 depletion indicate biological roles for PARP-7 in cell-cell adhesion and gene regulation. To identify the MARylated substrates of PARP-7 in ovarian cancer cells, we developed an NAD+ analog-sensitive approach, which we coupled with mass spectrometry to identify the PARP-7 ADP-ribosylated proteome in ovarian cancer cells, including cell-cell adhesion and cytoskeletal proteins. Specifically, we found that PARP-7 MARylates α-tubulin to promote microtubule instability, which may regulate ovarian cancer cell growth and motility. In sum, we identified an extensive PARP-7 ADP-ribosylated proteome with important roles in cancer-related cellular phenotypes.

Phytochemical concentrations and biological activities of Sorghum bicolor alcoholic extracts

2016 ◽  
Vol 7 (8) ◽  
pp. 3410-3420 ◽  
Author(s):  
Vermont P. Dia ◽  
Philipus Pangloli ◽  
Lynsey Jones ◽  
Angela McClure ◽  
Anjali Patel
Keyword(s):  
Ovarian Cancer ◽  
Antioxidant Activity ◽  
Sorghum Bicolor ◽  
Cancer Cells ◽  
Biological Activities ◽  
Ovarian Cancer Cells

Sorghum alcoholic extracts exhibited antioxidant activity and capability to inhibit and chemosensitize ovarian cancer cells in vitro.

scholarly journals 5, 7-Dihalo-8-quinolinol complex inhibits growth of ovarian cancer cells via the downregulation of expression of Wip1

2020 ◽  
Vol 19 (7) ◽  
pp. 1417-1422
Author(s):  
Rao Zhiwei ◽  
Xia Songbai ◽  
Han Qi
Keyword(s):  
Cell Cycle ◽  
Ovarian Cancer ◽  
Cancer Cells ◽  
Cytotoxic Effect ◽  
Ovarian Cancer Cell ◽  
Drug Candidate ◽  
Ovarian Cancer Cells ◽  
Cancer Cell Growth ◽  
Protein Expressions ◽  
G0 Phase

Purpose: To assess the cytotoxic effect of 5, 7-dihalo-8-quinolinol complex (DHQ) on ovarian cancer cells, and the mechanism of action involved.Methods: DHQ-mediated changes in cell viability were determined using MTT assay, while apoptosis was analyzed with flow cytometry. The effect of DHQ on cell migration was determined using inverted microscopy, while its effect on invasiveness was assessed with Giemsa dyeing. FACS Caliburinstrumentation was employed for analyzing the effect of DHQ on the cell cycle. The protein expressions of Wip1 and P53 were assayed by western blotting.Results: DHQ induced cytotoxicity against A2780 and OVCAR 3 cells in the concentration range of 0.25 - 12 μM (p < 0.05). In A2780 and OVCAR 3 cells, treatment with 12 μMDHQ resulted in 69.34 and 65.46 % apoptosis, respectively. The migratory potential and invasiveness of A2780 and OVCAR3 cells were significantly decreased by 12 μMDHQ, relative to untreated cells (p < 0.05). Moreover, treatment with 12 μMDHQ arrested cell cycle at G1/G0 phase in A2780 and OVCAR3 cells, but downregulated the protein expressions of Wip1 expression in A2780 and OVCAR3 cells.Conclusion: DHQ exerts cytotoxic effect on ovarian cancer cell growth via arrest of cell cycle and activation of apoptosis. Moreover, DHQ inhibits the migratory and invasive abilities of the cells. Thus, DHQ is a potential drug candidate for the management of ovarian cancer. Keywords: 5,7-Dihalo-8-quinolinol complex, Ovarian cancer, Cytotoxicity, Apoptosis, Invasiveness, Migration, Cell cycle

192 RESVERATROL, A NATURAL FOOD COMPOUND, SUPPRESSED THE CELL GROWTH OF BG-1 OVARIAN CANCER CELLS INDUCED BY 17β-ESTRADIOL OR BISPHENOL A THROUGH DOWNREGULATING ESTROGEN RECEPTOR α AND INSULIN-LIKE GROWTH FACTOR-1 RECEPTOR

2013 ◽  
Vol 25 (1) ◽  
pp. 245
Author(s):  
N.-H. Kang ◽  
K.-C. Choi
Keyword(s):  
Ovarian Cancer ◽  
Growth Factor ◽  
Cell Growth ◽  
Bisphenol A ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Ovarian Cancer Cell ◽  
Ovarian Cancer Cells ◽  
Insulin Like Growth Factor ◽  
Cancer Cell Growth

Resveratrol (trans-3,4,5-trihydroxystilbene; RES) was adopted in this study as a novel phytoestrogen displaying antioxidant, antiinflammatory, and anticancer effects. In this study, we evaluated the inhibitory effect of RES on the cell growth induced by 17β-oestradiol (E2), a typical oestrogen, and bisphenol A (BPA), an endocrine-disrupting chemical (EDC) in BG-1 ovarian cancer cells expressing oestrogen receptors (ER) through down-regulating oestrogen receptor α (ERa) and insulin-like growth factor-1 receptor (IGF-1R). The EDC and oestrogen appear to promote the development of the oestrogen-dependent cancers. Thus, we need to develop therapeutic methods for EDC-dependent cancers. In in vitro experiments, we examined the cell viability and mRNA expression of ERa ± IGF-1R genes following the treatments with E2 or BPA in the presence or absence of RES or ICI 182 780, an ER antagonist, by MTT assay and RT-PCR, respectively. We also examined the protein level of ERa, phosphorylated insulin receptor substrate-1 (IRS-1), phosphorylated Akt1/2/3, p21, and cyclin D1 by Western blot analysis. Treatment with E2 or BPA remarkably increased the growth of BG-1 ovarian cancer cells, and their enhanced cell growth appeared to be mediated by ERa. In addition, the treatment of BG-1 ovarian cancer cells with E2 or BPA resulted in an increase in ERa and IGF-1R gene expressions. However, co-treatment of RES reversed E2- or BPA-induced ovarian cancer cell growth and mRNA expressions of ERa and IGF-1R. The protein levels of phosphorylated IRS-1 and Akt were upregulated by E2 or BPA, whereas these levels were downregulated by co-treatment of RES in the presence of E2 or BPA. Taken together, these results indicate that RES may effectively inhibit ovarian cancer cell growth via downregulating cross-talk between ERa and IGF-1R. This work was supported by a National Research Foundation of Korea (NRF) grant funded by the Ministry of Education, Science and Technology (MEST) of Korea government (no. 2011-0015385).

scholarly journals Curcumin induces chemo/radio-sensitization in ovarian cancer cells and curcumin nanoparticles inhibit ovarian cancer cell growth

2010 ◽  
Vol 3 (1) ◽  
pp. 11 ◽  
Author(s):  
Murali M Yallapu ◽  
Diane M Maher ◽  
Vasudha Sundram ◽  
Maria C Bell ◽  
Meena Jaggi ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Cell Growth ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Ovarian Cancer Cell ◽  
Ovarian Cancer Cells ◽  
Cancer Cell Growth ◽  
Curcumin Nanoparticles

scholarly journals ETV5 transcription factor is overexpressed in ovarian cancer and regulates cell adhesion in ovarian cancer cells

2011 ◽  
Vol 130 (7) ◽  
pp. 1532-1543 ◽  
Author(s):  
Marta Llauradó ◽  
Miguel Abal ◽  
Josep Castellví ◽  
Sílvia Cabrera ◽  
Antonio Gil-Moreno ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Transcription Factor ◽  
Cell Adhesion ◽  
Cancer Cells ◽  
Ovarian Cancer Cells

scholarly journals Epidermal Growth Factor-Induced GnRH-II Synthesis Contributes to Ovarian Cancer Cell Invasion

2009 ◽  
Vol 94 (9) ◽  
pp. 3618-3618
Author(s):  
Song Ling Poon ◽  
Gareth T. Hammond ◽  
Peter C. K. Leung
Keyword(s):  
Ovarian Cancer ◽  
Cancer Cells ◽  
Promoter Activity ◽  
Binding Protein ◽  
Ovarian Cancer Cells ◽  
Mrna Levels ◽  
Upstream Regulator ◽  
Enhancer Binding Protein ◽  
Responsive Element ◽  
Interfering Rna

GnRH-II modulates ovarian cancer cells invasion and is expressed in normal ovary and ovarian epithelial cancer cells; however, the upstream regulator(s) of GnRH-II expression in these cells remains unclear. We now demonstrate that epidermal growth factor (EGF) increases GnRH-II mRNA levels in several human ovarian carcinoma cell lines and up-regulates GnRH-II promoter activity in OVCAR-3 cells in a dose-dependent manner, whereas an EGF receptor inhibitor (AG148) abolishes EGF-induced increases in GnRH-II promoter activity and GnRH-II mRNA levels. EGF increases the phosphorylation of cAMP-responsive element-binding protein (p-CREB) and its association with the coregulator, CCAAT/enhancer binding protein β, whereas blocking the EGF-induced ERK1/2 phosphorylation with MAPK inhibitors (PD98059/U0126) markedly reduced these effects. Moreover, depletion of CREB using small interfering RNA attenuated EGF-induced GnRH-II promoter activity. Chromatin immunoprecipitation assays demonstrated that EGF induces p-CREB binding to a cAMP responsive-element within the GnRH-II promoter, likely in association with CCAAT/enhancer binding protein β, and mutagenesis of this cAMP responsive-element prevented EGF-induced GnRH-II promoter activity in OVCAR-3 cells. Importantly, GnRH-II acts additively with EGF to promote invasion of OVCAR-3 and CaOV-3 cells, but not SKOV-3 cells that express low levels of GnRH receptor (GnRHR). Treatment with GnRHR small interfering RNA also partially inhibited the EGF-induced invasion of OVCAR-3 and CaOV-3 cells. Furthermore, EGF treatment transiently increases GnRHR levels in OVCAR-3 and CaOV-3, which likely accentuates the effects of increase GnRH-II production on cell invasion. These results provide evidence that EGF is an upstream regulator of the autocrine actions of GnRH-II on the invasive properties of ovarian cancer cells.

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