scholarly journals TNFAIP8 promotes cell growth by regulating the Hippo pathway in epithelial ovarian cancer

2018 ◽  
Author(s):  
Yao Xie ◽  
Fei Zhou ◽  
Xia Zhao
Keyword(s):  
Ovarian Cancer ◽  
Cell Growth ◽  
Epithelial Ovarian Cancer ◽  
Hippo Pathway ◽  
The Hippo Pathway

Abstract PO-132: Upregulated LYL1 promotes epithelial ovarian cancer (EOC) cell growth and metastasis

2022 ◽  
Author(s):  
Damieanus Ochola ◽  
Shirisha Jonnalagadda ◽  
Swetha Peddibhotla ◽  
Tasmin Omy ◽  
Mark Reedy ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Cell Growth ◽  
Epithelial Ovarian Cancer

scholarly journals Staurosporine targets the Hippo pathway to inhibit cell growth

2018 ◽  
Vol 10 (3) ◽  
pp. 267-269
Author(s):  
Xueyan Ma ◽  
Peixue Li ◽  
Peihao Chen ◽  
Jinhui Li ◽  
Hongling Huang ◽  
...  
Keyword(s):  
Cell Growth ◽  
Hippo Pathway ◽  
Inhibit Cell Growth ◽  
The Hippo Pathway

scholarly journals miR-363 confers taxane resistance in ovarian cancer by targeting the Hippo pathway member, LATS2

Oncotarget ◽  
2018 ◽  
Vol 9 (53) ◽  
pp. 30053-30065 ◽  
Author(s):  
Zeinab Mohamed ◽  
Mohamed Kamel Hassan ◽  
Safwat Okasha ◽  
Takashi Mitamura ◽  
Sarah Keshk ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Hippo Pathway ◽  
Taxane Resistance ◽  
The Hippo Pathway

scholarly journals Downregulation of MYPT1 increases tumor resistance in ovarian cancer by targeting the Hippo pathway and increasing the stemness

2020 ◽  
Vol 19 (1) ◽  
Author(s):  
Sandra Muñoz-Galván ◽  
Blanca Felipe-Abrio ◽  
Eva M. Verdugo-Sivianes ◽  
Marco Perez ◽  
Manuel P. Jiménez-García ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Molecular Mechanisms ◽  
Target Genes ◽  
Hippo Pathway ◽  
Ovarian Tumors ◽  
Tumor Resistance ◽  
Functional Link ◽  
The Hippo Pathway

Abstract Background Ovarian cancer is one of the most common and malignant cancers, partly due to its late diagnosis and high recurrence. Chemotherapy resistance has been linked to poor prognosis and is believed to be linked to the cancer stem cell (CSC) pool. Therefore, elucidating the molecular mechanisms mediating therapy resistance is essential to finding new targets for therapy-resistant tumors. Methods shRNA depletion of MYPT1 in ovarian cancer cell lines, miRNA overexpression, RT-qPCR analysis, patient tumor samples, cell line- and tumorsphere-derived xenografts, in vitro and in vivo treatments, analysis of data from ovarian tumors in public transcriptomic patient databases and in-house patient cohorts. Results We show that MYPT1 (PPP1R12A), encoding myosin phosphatase target subunit 1, is downregulated in ovarian tumors, leading to reduced survival and increased tumorigenesis, as well as resistance to platinum-based therapy. Similarly, overexpression of miR-30b targeting MYPT1 results in enhanced CSC-like properties in ovarian tumor cells and is connected to the activation of the Hippo pathway. Inhibition of the Hippo pathway transcriptional co-activator YAP suppresses the resistance to platinum-based therapy induced by either low MYPT1 expression or miR-30b overexpression, both in vitro and in vivo. Conclusions Our work provides a functional link between the resistance to chemotherapy in ovarian tumors and the increase in the CSC pool that results from the activation of the Hippo pathway target genes upon MYPT1 downregulation. Combination therapy with cisplatin and YAP inhibitors suppresses MYPT1-induced resistance, demonstrating the possibility of using this treatment in patients with low MYPT1 expression, who are likely to be resistant to platinum-based therapy.

scholarly journals MiR-596 activated by EP300 controls the tumorigenesis in epithelial ovarian cancer by declining BRD4 and KPNA4

2020 ◽  
Vol 20 (1) ◽  
Author(s):  
Deying Wang ◽  
Yulan Cui ◽  
Aili Xu ◽  
Lin Zhao ◽  
Peiling Li
Keyword(s):  
Ovarian Cancer ◽  
Cell Proliferation ◽  
Cell Growth ◽  
Epithelial Ovarian Cancer ◽  
Luciferase Reporter ◽  
Past Study ◽  
Protein Levels ◽  
Promising Therapeutic Target ◽  
Advanced Stages

Abstract Background Epithelial ovarian cancer (EOC), a subclass of ovarian cancer (OC), is usually diagnosed at advanced stages due to the lack of effective screening means. Mounting reports have disclosed the vitally important roles of microRNAs (miRNAs) in carcinogenesis. Here, we aimed to find out possible miRNAs participating in EOC development. Methods qRT-PCR ad western blot respectively examined the mRNA and protein levels of studied genes. CCK-8, colony formation, flow cytometry, TUNEL and spheroid formation assays were appropriately employed for examining cell proliferation, cell cycle, apoptosis and stemness. The interaction between molecules was affirmed by luciferase reporter, RNA pull down and ChIP assays. Results In consistent with the observation of a past study, miR-596 expression was relatively low in EOC cells. Up-regulating miR-596 suppressed EOC cell proliferation and stemness. EP300 transcriptionally activated miR-596 to serve as a tumor-repressor in EOC. Then BRD4 and KPNA4, whose knockdown led to restraining effects on cell growth and stemness, were both revealed to be targeted by miR-596 in EOC. Lastly, rescue assays affirmed the tumor-restraining role of miR-596-BRD4/KPNA4 axis in EOC. Conclusion EP300-activated miR-596 hampered cell growth and stemness via targeting BRD4 and KPNA4 in EOC, proofing miR-596 as a promising therapeutic target in treating EOC patients.

scholarly journals Krupple-Like Factor 5 is a Potential Therapeutic Target and Prognostic Marker in Epithelial Ovarian Cancer

2020 ◽  
Vol 11 ◽  
Author(s):  
Abdul K. Siraj ◽  
Poyil Pratheeshkumar ◽  
Sasidharan Padmaja Divya ◽  
Sandeep Kumar Parvathareddy ◽  
Khadija A. Alobaisi ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Cell Growth ◽  
Epithelial Ovarian Cancer ◽  
Signaling Pathway ◽  
Cell Lines ◽  
Therapeutic Target ◽  
Potential Therapeutic Target ◽  
Mesenchymal Transition ◽  
Stat3 Signaling ◽  
Stat3 Signaling Pathway

Epithelial ovarian cancer (EOC) is the most lethal gynecological malignancy. Despite current therapeutic and surgical options, advanced EOC shows poor prognosis. Identifying novel molecular therapeutic targets is highly needed in the management of EOC. Krupple-like factor 5 (KLF5), a zinc-finger transcriptional factor, is highly expressed in a variety of cancer types. However, its role and expression in EOC is not fully illustrated. Immunohistochemical analysis was performed to assess KLF5 protein expression in 425 primary EOC samples using tissue microarray. We also addressed the function of KLF5 in EOC and its interaction with signal transducer and activator of transcription 3 (STAT3) signaling pathway. We found that KLF5 overexpressed in 53% (229/425) of EOC samples, and is associated with aggressive markers. Forced expression of KLF5 enhanced cell growth in low expressing EOC cell line, MDAH2774. Conversely, knockdown of KLF5 reduced cell growth, migration, invasion and progression of epithelial to mesenchymal transition in KLF5 expressing cell lines, OVISE and OVSAHO. Importantly, silencing of KLF5 decreased the self-renewal ability of spheroids generated from OVISE and OVSAHO cell lines. In addition, downregulation of KLF5 potentiated the effect of cisplatin to induce apoptosis in these cell lines. These data reveals the pro-tumorigenic role of KLF5 in EOC and uncover its role in activation of STAT3 signaling pathway, suggesting the importance of KLF5 as a potential therapeutic target for EOC therapy.

Inhibition of Human Epithelial Ovarian Cancer Cell Growth in vitro by Somatostatin Analog RC-160

Oncology ◽  
2000 ◽  
Vol 59 (Suppl. 1) ◽  
pp. 45-49 ◽  
Author(s):  
Tetsu Yano ◽  
Sinisa Radulovic ◽  
Yutaka Osuga ◽  
Koji Kugu ◽  
Hiroyuki Yoshikawa ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Cell Growth ◽  
Epithelial Ovarian Cancer ◽  
Cancer Cell ◽  
Ovarian Cancer Cell ◽  
Somatostatin Analog ◽  
Epithelial Ovarian Cancer Cell ◽  
Cancer Cell Growth
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