Regulation of cadherins and catenins in ovarian surface epithelium and ovarian cancer

2007 ◽  
Author(s):  
Yuen-lam Pon
Keyword(s):  
Ovarian Cancer ◽  
Ovarian Surface Epithelium ◽  
Surface Epithelium ◽  
Ovarian Surface

Spontaneous transformation of the ovarian surface epithelium and the biology of ovarian cancer

1995 ◽  
pp. 145-156 ◽  
Author(s):  
H. Salazar ◽  
A. K. Godwin ◽  
L. A. Getts ◽  
J. R. Testa ◽  
M. Daly ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Ovarian Surface Epithelium ◽  
Surface Epithelium ◽  
Spontaneous Transformation ◽  
Ovarian Surface

scholarly journals Ovarian Surface Epithelium: Biology, Endocrinology, and Pathology*

2001 ◽  
Vol 22 (2) ◽  
pp. 255-288 ◽  
Author(s):  
Nelly Auersperg ◽  
Alice S. T. Wong ◽  
Kyung-Chul Choi ◽  
Sung Keun Kang ◽  
Peter C. K. Leung
Keyword(s):  
Ovarian Cancer ◽  
Molecular Mechanisms ◽  
Ovarian Surface Epithelium ◽  
Surface Epithelium ◽  
Neoplastic Progression ◽  
Ovarian Carcinomas ◽  
Genetic Changes ◽  
Ovarian Surface ◽  
Histological Characteristics ◽  
Epithelial Ovarian Carcinomas

Abstract The epithelial ovarian carcinomas, which make up more than 85% of human ovarian cancer, arise in the ovarian surface epithelium (OSE). The etiology and early events in the progression of these carcinomas are among the least understood of all major human malignancies because there are no appropriate animal models, and because methods to culture OSE have become available only recently. The objective of this article is to review the cellular and molecular mechanisms that underlie the control of normal and neoplastic OSE cell growth, differentiation, and expression of indicators of neoplastic progression. We begin with a brief discussion of the development of OSE, from embryonic to the adult. The pathological and genetic changes of OSE during neoplastic progression are next summarized. The histological characteristics of OSE cells in culture are also described. Finally, the potential involvement of hormones, growth factors, and cytokines is discussed in terms of their contribution to our understanding of the physiology of normal OSE and ovarian cancer development.

scholarly journals Inactivation of TRP53, PTEN, RB1, and/or CDH1 in the ovarian surface epithelium induces ovarian cancer transformation and metastasis

2020 ◽  
Vol 102 (5) ◽  
pp. 1055-1064 ◽  
Author(s):  
Mingxin Shi ◽  
Allison E Whorton ◽  
Nikola Sekulovski ◽  
Marilène Paquet ◽  
James A MacLean ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Ovarian Surface Epithelium ◽  
Genetically Engineered ◽  
Surface Epithelium ◽  
Low Grade ◽  
Type I ◽  
Epithelial Hyperplasia ◽  
Genetically Engineered Mouse Models ◽  
Ovarian Surface ◽  
Tumor Dissemination

Abstract Ovarian cancer (OvCa) remains the most common cause of death from gynecological malignancies. Genetically engineered mouse models have been used to study initiation, origin, progression, and/or mechanisms of OvCa. Based on the clinical features of OvCa, we examined a quadruple combination of pathway perturbations including PTEN, TRP53, RB1, and/or CDH1. To characterize the cancer-promoting events in the ovarian surface epithelium (OSE), Amhr2cre/+ mice were used to ablate floxed alleles of Pten, Trp53, and Cdh1, which were crossed with TgK19GT121 mice to inactivate RB1 in KRT19-expressing cells. Inactivation of PTEN, TRP53, and RB1 with or without CDH1 led to the development of type I low-grade OvCa with enlarged serous papillary carcinomas and some high-grade serous carcinomas (HGSCs) in older mice. Initiation of epithelial hyperplasia and micropapillary carcinoma started earlier at 1 month in the triple mutations of Trp53, Pten, and Rb1 mice as compared to 2 months in quadruple mutations of Trp53, Pten, Rb1, and Cdh1 mice, whereas both genotypes eventually developed enlarged proliferating tumors that invaded into the ovary at 3–4 months. Mice with triple and quadruple mutations developed HGSC and/or metastatic tumors, which disseminated into the peritoneal cavity at 4–6 months. In summary, inactivation of PTEN, TRP53, and RB1 initiates OvCa from the OSE. Additional ablation of CDH1 further increased persistence of tumor dissemination and ascites fluid accumulation enhancing peritoneal metastasis.

scholarly journals Loss of LKB1 and PTEN tumor suppressor genes in the ovarian surface epithelium induces papillary serous ovarian cancer

2013 ◽  
Vol 35 (3) ◽  
pp. 546-553 ◽  
Author(s):  
Pradeep S. Tanwar ◽  
Gayatry Mohapatra ◽  
Sarah Chiang ◽  
David A. Engler ◽  
LiHua Zhang ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Tumor Suppressor ◽  
Tumor Suppressor Genes ◽  
Ovarian Surface Epithelium ◽  
Surface Epithelium ◽  
Serous Ovarian Cancer ◽  
Suppressor Genes ◽  
Ovarian Surface

scholarly journals Autocrine Interactions of Keratinocyte Growth Factor, Hepatocyte Growth Factor, and Kit-Ligand in the Regulation of Normal Ovarian Surface Epithelial Cells*

Endocrinology ◽  
2000 ◽  
Vol 141 (7) ◽  
pp. 2532-2539 ◽  
Author(s):  
Jeff A. Parrott ◽  
Rachel Mosher ◽  
Grace Kim ◽  
Michael K. Skinner
Keyword(s):  
Ovarian Cancer ◽  
Growth Factors ◽  
Growth Factor ◽  
Hepatocyte Growth Factor ◽  
Keratinocyte Growth Factor ◽  
Ovarian Surface Epithelium ◽  
Surface Epithelium ◽  
Kit Ligand ◽  
Ovarian Surface ◽  
Hepatocyte Growth

Ovarian tumors are primarily derived from the layer of epithelium surrounding the ovary termed the ovarian surface epithelium (OSE). Although extensive research has focused on established ovarian tumors, relatively little is known about the normal biology of the OSE that gives rise to ovarian cancer. The local expression and actions of growth factors are likely involved in both normal and tumorigenic OSE biology. The current study investigates the expression and action of keratinocyte growth factor (KGF), hepatocyte growth factor (HGF), and kit-ligand (KL) in normal ovarian surface epithelium (OSE). The actions of various growth factors on KGF, HGF, and KL expression are examined. Observations indicate that freshly isolated normal OSE express the genes for KGF, HGF, and KL and expression is maintained in vitro. KGF messenger RNA expression in OSE was found to be stimulated by KGF and HGF, but not KL. HGF expression in OSE was found to be stimulated by KGF, HGF, and KL. KL expression in OSE was also found to be stimulated by KGF, HGF, and KL. Therefore, the various growth factors can regulate the mRNA expression of each other in OSE. Effects of growth factors on OSE growth were examined. KGF, HGF, and KL stimulated OSE growth to similar levels as the positive control epidermal growth factor. Observations suggest that KGF, HGF, and KL interact to promote OSE growth and growth factor expression. The ability of these growth factors to interact in a positive autocrine feedback loop is postulated to be important for normal OSE biology. Paracrine interactions with the adjacent stromal cells will also be a factor in OSE biology. Abnormal interactions of these growth factors may be involved in the onset and progression of ovarian cancer.

scholarly journals Loss of GATA6 Leads to Nuclear Deformation and Aneuploidy in Ovarian Cancer

2009 ◽  
Vol 29 (17) ◽  
pp. 4766-4777 ◽  
Author(s):  
Callinice D. Capo-chichi ◽  
Kathy Q. Cai ◽  
Joseph R. Testa ◽  
Andrew K. Godwin ◽  
Xiang-Xi Xu
Keyword(s):  
Ovarian Cancer ◽  
Nuclear Envelope ◽  
Cancer Cells ◽  
Human Cancer ◽  
Ovarian Surface Epithelium ◽  
Surface Epithelium ◽  
Ovarian Cancer Cells ◽  
Ovarian Surface ◽  
Ovarian Surface Epithelial ◽  
Ovarian Tumorigenesis

ABSTRACT A prominent hallmark of most human cancer is aneuploidy, which is a result of the chromosomal instability of cancer cells and is thought to contribute to the initiation and progression of most carcinomas. The developmentally regulated GATA6 transcription factor is commonly lost in ovarian cancer, and the loss of its expression is closely associated with neoplastic transformation of the ovarian surface epithelium. In the present study, we found that reduction of GATA6 expression with small interfering RNA (siRNA) in human ovarian surface epithelial cells resulted in deformation of the nuclear envelope, failure of cytokinesis, and formation of polyploid and aneuploid cells. We further discovered that loss of the nuclear envelope protein emerin may mediate the consequences of GATA6 suppression. The nuclear phenotypes were reproduced by direct suppression of emerin with siRNA. Thus, we conclude that diminished expression of GATA6 leads to a compromised nuclear envelope that is causal for polyploidy and aneuploidy in ovarian tumorigenesis. The loss of emerin may be the basis of nuclear morphological deformation and subsequently the cause of aneuploidy in ovarian cancer cells.

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