OCT4 controls mitotic stability and inactivates the RB tumor suppressor pathway to enhance ovarian cancer aggressiveness

Oncogene ◽  
2017 ◽  
Vol 36 (30) ◽  
pp. 4253-4266 ◽  
Author(s):  
E Comisso ◽  
M Scarola ◽  
M Rosso ◽  
S Piazza ◽  
S Marzinotto ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Tumor Suppressor ◽  
Mitotic Stability ◽  
Cancer Aggressiveness

scholarly journals VGLL3 expression is associated with a tumor suppressor phenotype in epithelial ovarian cancer

2013 ◽  
Vol 7 (3) ◽  
pp. 513-530 ◽  
Author(s):  
Karen Gambaro ◽  
Michael C.J. Quinn ◽  
Paulina M. Wojnarowicz ◽  
Suzanna L. Arcand ◽  
Manon de Ladurantaye ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Tumor Suppressor ◽  
Epithelial Ovarian Cancer

OPCML at 11q25 is epigenetically inactivated and has tumor-suppressor function in epithelial ovarian cancer

2003 ◽  
Vol 34 (3) ◽  
pp. 337-343 ◽  
Author(s):  
Grant C Sellar ◽  
Karen P Watt ◽  
Genevieve J Rabiasz ◽  
Euan A Stronach ◽  
Li Li ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Tumor Suppressor ◽  
Epithelial Ovarian Cancer ◽  
Tumor Suppressor Function ◽  
Suppressor Function

scholarly journals Discoidin Domain Receptor 2 Mediates Lysophosphatidic Acid-Induced Ovarian Cancer Aggressiveness

2021 ◽  
Vol 22 (10) ◽  
pp. 5374
Author(s):  
Bo Young Jeong ◽  
Kyung Hwa Cho ◽  
Se-Hee Yoon ◽  
Chang Gyo Park ◽  
Hwan-Woo Park ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Cancer Cell ◽  
Lysophosphatidic Acid ◽  
Cell Invasion ◽  
Ovarian Cancer Cell ◽  
Ovarian Cancer Cells ◽  
Cancer Cell Invasion ◽  
Discoidin Domain Receptor ◽  
Cancer Aggressiveness ◽  
Discoidin Domain Receptor 2

Lysophosphatidic acid (LPA), a bioactive lipid produced extracellularly by autotaxin (ATX), has been known to induce various pathophysiological events, including cancer cell invasion and metastasis. Discoidin domain receptor 2 (DDR2) expression is upregulated in ovarian cancer tissues, and is closely associated with poor clinical outcomes in ovarian cancer patients. In the present study, we determined a critical role and signaling cascade for the expression of DDR2 in LPA-induced ovarian cancer cell invasion. We also found ectopic expression of ATX or stimulation of ovarian cancer cells with LPA-induced DDR2 expression. However, the silencing of DDR2 expression significantly inhibited ATX- and LPA-induced ovarian cancer cell invasion. In addition, treatment of the cells with pharmacological inhibitors of phosphoinositide 3-kinase (PI3K), Akt, and mTOR abrogated LPA-induced DDR2 expression. Moreover, we observed that HIF-1α, located downstream of the mTOR, is implicated in LPA-induced DDR2 expression and ovarian cancer cell invasion. Finally, we provide evidence that LPA-induced HIF-1α expression mediates Twist1 expression to upregulate DDR2 expression. Collectively, the present study demonstrates that ATX, and thereby LPA, induces DDR2 expression through the activation of the PI3K/Akt/mTOR/HIF-1α/Twist1 signaling axes, aggravating ovarian cancer cell invasion.

scholarly journals Correction: Potential Role of Estrogen Receptor Beta as a Tumor Suppressor of Epithelial Ovarian Cancer

PLoS ONE ◽  
2013 ◽  
Vol 8 (5) ◽  
Author(s):  
Carine Bossard ◽  
Muriel Busson ◽  
David Vindrieux ◽  
Françoise Gaudin ◽  
Véronique Machelon ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Estrogen Receptor ◽  
Tumor Suppressor ◽  
Epithelial Ovarian Cancer ◽  
Potential Role ◽  
Estrogen Receptor Beta ◽  
Receptor Beta ◽  
Correction Potential

scholarly journals CircPLEKHM3 acts as a tumor suppressor through regulation of the miR-9/BRCA1/DNAJB6/KLF4/AKT1 axis in ovarian cancer

2019 ◽  
Vol 18 (1) ◽  
Author(s):  
Lei Zhang ◽  
Qing Zhou ◽  
Qiongzi Qiu ◽  
Ling Hou ◽  
Mengting Wu ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Tumor Suppressor ◽  
Cancer Cells ◽  
Cancer Patients ◽  
Cancer Biology ◽  
Ovarian Cancer Cells ◽  
Ovarian Carcinomas ◽  
Mesenchymal Transition ◽  
Normal Tissues ◽  
Endogenous Expression

Abstract Background Emerging evidence has shown that circular RNAs (circRNAs) play essential roles in cancer biology and are potential biomarkers and targets for cancer therapy. However, the expression and function of circRNAs in ovarian carcinogenesis and its progression remain elusive. Methods RNA sequencing was performed to reveal circRNA expression profiles in ovarian cancerous and normal tissues. Single-molecule RNA in-situ hybridization was used to quantify circPLEKHM3 expression in tumor tissues. Cell-based in-vitro and in-vivo assays were subsequently conducted to support the clinical findings. Results CircPLEKHM3 was identified as one of the most significantly down-regulated circRNAs in ovarian cancer tissues compared with normal tissues. Its expression was further decreased in peritoneal metastatic ovarian carcinomas compared to primary ovarian carcinomas. Patients with lower circPLEKHM3 tend to have a worse prognosis. Functionally, circPLEKHM3 overexpression inhibited cell growth, migration and epithelial–mesenchymal transition, whereas its knockdown exerted an opposite role. Further analyses showed that circPLEKHM3 sponged miR-9 to regulate the endogenous expression of BRCA1, DNAJB6 and KLF4, and consequently inactivate AKT1 signaling. In addition, AKT inhibitor MK-2206 could block the tumor-promoting effect of circPLEKHM3 depletion, and potentiate Taxol-induced growth inhibition of ovarian cancer cells. Conclusions Our findings demonstrated that circPLEKHM3 functions as a tumor suppressor in ovarian cancer cells by targeting the miR-9/BRCA1/DNAJB6/KLF4/AKT1 axis and may be used as a prognostic indicator and therapeutic target in ovarian cancer patients. The new strategy for treating ovarian cancer by a combination therapy of Taxol with MK-2206 is worth further investigation, especially in ovarian cancer patients with loss of circPLEKHM3 expression.

Abstract 1579: Matrix metalloproteinase 1: Oncogene or tumor suppressor in ovarian cancer

2020 ◽  
Author(s):  
Zhiqing Huang ◽  
Cassie Hobbs ◽  
Olivia Neely ◽  
Derek Y. Yao ◽  
Junhee Shin ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Tumor Suppressor ◽  
Matrix Metalloproteinase ◽  
Matrix Metalloproteinase 1
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