scholarly journals Telomerase in the ovary

Reproduction ◽  
2010 ◽  
Vol 140 (2) ◽  
pp. 215-222 ◽  
Author(s):  
Jun-Ping Liu ◽  
He Li
Keyword(s):  
Ovarian Cancer ◽  
Germ Cells ◽  
Granulosa Cells ◽  
Reproductive Function ◽  
Ovarian Surface Epithelium ◽  
Malignant Cell ◽  
Telomerase Activity ◽  
Ovary Development ◽  
Surface Epithelium ◽  
Neoplastic Cells

Telomerase, an enzyme complex that binds the chromosome ends (telomeres) and maintains telomere length and integrity, is present in germ cells, proliferative granulosa cells, germline stem cells, and neoplastic cells in the ovary, but it is absent in differentiated or aged cells. Activation of telomerase in the ovary underpins both benign and malignant cell proliferation in several compartments, including the germ cells, membrana granulosa, and the ovarian surface epithelium. The difference in telomerase operation between normal and abnormal cell proliferations may lie in the mechanisms of telomerase activation in a deregulated manner. Recent studies have implicated telomerase activity in ovarian cancer as well as oogenesis and fertility. Inhibition of telomerase and the shortening of telomeres are seen in occult ovarian insufficiency. Studies of how telomerase operates and regulates ovary development may provide insight into the development of both germ cells for ovarian reproductive function and neoplastic cells in ovarian cancer. The current review summarizes the roles of telomerase in the development of oocytes and proliferation of granulosa cells during folliculogenesis and in the process of tumorigenesis. It also describes the regulation of telomerase by estrogen in the ovary.

scholarly journals Estrogen Receptor Alpha (ER-α) and Beta (ER-β) mRNAs in Normal Ovary, Ovarian Serous Cystadenocarcinoma and Ovarian Cancer Cell Lines: Down-Regulation of ER-β in Neoplastic Tissues

1998 ◽  
Vol 83 (3) ◽  
pp. 1025-1028 ◽  
Author(s):  
Alfred W. Brandenberger ◽  
Meng Kian Tee ◽  
Roberts B. Jaffe
Keyword(s):  
Ovarian Cancer ◽  
Estrogen Receptor ◽  
Granulosa Cells ◽  
Ovarian Cancer Cell ◽  
Ovarian Surface Epithelium ◽  
Surface Epithelium ◽  
Mrna Levels ◽  
Rt Pcr ◽  
Low Level ◽  
Ovarian Cancer Cell Lines

The prognosis in ovarian carcinoma, the most lethal of the gynecologic neoplasms, is poor and has changed little in the last three decades. Only a small number respond to antiestrogen therapy, although the classic estrogen receptor, ER-α, has been identified in ovarian surface epithelium, from which approximately 90% of ovarian cancers originate. We have previously shown that ER-β mRNA is most abundant in human fetal ovaries, suggesting that it might play an important role in ovarian development. Therefore, we investigated the mRNA levels of both ERs in normal ovaries, ovarian serous cystadenocarcinomas, granulosa cells from patients undergoing in vitro fertilization (IVF), the ovarian surface epithelium cell line IOSE-Van, and the ovarian cancer cell lines SKOV3, HEY and OCC1. Northern blots of normal and neoplastic ovaries were hybridized with an ER-β riboprobe that spans the A/B domain. We detected two major hybridizing bands at approximately 8 and 10 kb. An RNase protection assay using the same probe revealed a single band of the expected size. Hybridizing the same blot with an ER-α riboprobe showed a strong hybridizing band at approximately 6.5 kb. In ovarian cancer samples, ER-β mRNA level was decreased when compared to normal ovaries. Using 25 cycles of RT-PCR followed by Southern blotting, we found equal amounts of ER-α and -β mRNAs in normal ovaries in all age groups from 33 to 75 years; however, in ovarian cancer tissue, the level of ER-α mRNA was similar or slightly higher, comparable to 103 to 104 copies of plasmid DNA, but ER-β mRNA levels were markedly decreased. Granulosa cells from IVF patients expressed high levels of ER-β mRNA. The OSE cell line expressed low level of ER-α, detectable after 40 cycles of RT-PCR and no ER-β mRNA. SKOV3, showed low level of ER-α and β mRNAs, whereas OCC1 showed low level of ER-β and relatively high level of ER-α. HEY did not contain detectable amounts of either ER after 40 cycles of RT-PCR. We found no evidence of differential splicing or major deletions in almost the entire coding region of ER-β in either normal ovaries or tumor samples.

Post-natal oogenesis: a concept for controversy that intensified during the last decade

Zygote ◽  
2013 ◽  
Vol 23 (3) ◽  
pp. 315-326 ◽  
Author(s):  
Yashar Esmaeilian ◽  
Arzu Atalay ◽  
Esra Erdemli
Keyword(s):  
Stem Cells ◽  
Bone Marrow ◽  
Immune System ◽  
Germ Cells ◽  
Granulosa Cells ◽  
Ovarian Surface Epithelium ◽  
Surface Epithelium ◽  
Germline Stem Cells ◽  
Ovarian Stem Cells ◽  
Hormonal Signalling

SummaryFor decades, scientists have considered that female mammals are born with a lifetime reserve of oocytes in the ovary, irrevocably fated to decline after birth. However, controversy in the matter of the possible presence of oocytes and granulosa cells that originate from stem cells in the adult mammalian ovaries has been expanded. The restricted supply of oocytes in adult female mammals has been disputed in recent years by supporters of neo-oogenesis, who claim that germline stem cells (GSCs) exist in the ovarian surface epithelium (OSE) or the bone marrow (BM). Differentiation of ovarian stem cells (OSCs) into oocytes, fibroblast-like cells, granulosa phenotype, neural and mesenchymal type cells and generation of germ cells from OSCs under the contribution of an OSC niche that consists of immune system-related cells and hormonal signalling has been claimed. Although these arguments have met with intense suspicion, their confirmation would necessitate the revision of the current classic knowledge of female reproductive biology.

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

Ovarian Cancer Cell Invasiveness Correlates With Increased Cell Deformability

2012 ◽  
Author(s):  
Wenwei Xu ◽  
Roman Mezencev ◽  
Byungkyu Kim ◽  
Lijuan Wang ◽  
John McDonald ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Cancer Cells ◽  
Single Cells ◽  
Metastatic Cancer ◽  
Ovarian Surface Epithelium ◽  
Surface Epithelium ◽  
Ovarian Cancer Cells ◽  
Cell Deformability ◽  
Ovarian Cells ◽  
And Migration

Cancer cells undergo a variety of biochemical and biophysical transformations when compared to identical cells displaying a healthy phenotypic state, cancer cells show a drastic reduction of stiffness upon malignancy[1, 2] and change of stiffness of single cells can indicate the presence of disease [3–6]. Besides, metastatic cancer has a higher deformability than their benign counterparts[7, 8]. Using atomic force microscopy, we demonstrated that cancerous ovarian cells (OVCAR3, OVCAR4, HEY and HEYA8) are substantially softer than the healthy immortalized ovarian surface epithelium (IOSE) cells. In addition, within the different types of cancerous ovarian cells, increased invasiveness and migration are directly correlated with increased cell deformability. These results indicate that stiffness of individual cells can distinguish not only ovarian cancer cells from healthy cells types, but also invasive cancer types from less invasive types. Stiffness may provide an alternative and convenient biomarker to grade the metastasis potential of cancer cells.

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

Spatiotemporal changes in cytokeratin expression in the neonatal rat ovary

1998 ◽  
Vol 76 (1) ◽  
pp. 27-35 ◽  
Author(s):  
Jie Pan ◽  
Nelly Auersperg
Keyword(s):  
Granulosa Cells ◽  
Zona Pellucida ◽  
Basal Membrane ◽  
Ovarian Surface Epithelium ◽  
Hydroxysteroid Dehydrogenase ◽  
Collagen Iv ◽  
Basement Membranes ◽  
Neonatal Rat ◽  
Surface Epithelium ◽  
Collagen Type Iv

Ovarian granulosa cells are derived embryologically from two keratin-positive epithelia of mesodermal origin, the ovarian rete and the ovarian surface epithelium. In the rat, presumptive granulosa cells still express keratin at birth but as they acquire functions related to oocyte support and steroidogenesis in the maturing ovary they lose this epithelial differentiation marker. Using double-label immunofluorescence microscopy, we examined the distribution of keratin-expressing granulosa cells in rat ovaries on days 1-10 postpartum in relation to (i) laminin and collagen type IV in follicular basement membranes, (ii) the zona pellucida, and (iii) 3β-hydroxysteroid dehydrogenase activity. Keratin was present in most (pre)granulosa cells on days 1-3. As the cells became multilayered in growing follicles, keratin was retained by granulosa cells adjacent to follicular basement membranes but disappeared from cells that were displaced towards follicular centers. From day 7 on, large follicles lacked keratin altogether. Laminin was a consistent component of follicular basement membranes at all ages, while collagen IV varied and diminished in parallel with keratin. 3β-Hydroxysteroid dehydrogenase was demonstrable in stromal interstitial cells from day 7 on. Zona pellucida first appeared in primary follicles adjacent to keratin-positive cells and subsequently became surounded with keratin-negative granulosa cells in growing follicles. The results suggest different roles for laminin and collagen IV in follicular basement membranes and support the hypothesis that keratin expression by granulosa cells depends on paracrine interactions with the ovarian stroma. In early growing follicles, these interactions may be interrupted by physical removal from the vicinity of the basement membranes as the granulosa cells become multilayered. In the more mature follicles, the loss of keratin from all granulosa cells suggests that the required stromal signals cease, perhaps as the perifollicular stroma differentiates into the theca.Key words: ovary, differentiation, keratin, basal membrane, development.

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