Enzymes of estrogen metabolism in endometrial cancer

Бочкарева, Н. В.; Kolomiets, L. А.; Kondakova, I. V.; Стуканов, С. Л.; Старова, А. Б.; Агаркова, Л. А.

doi:10.1007/s10517-006-0138-8

Cited by 8 publications

(4 citation statements)

References 3 publications

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“…Regarding tumors, the presence of aromatase has already been described in breast cancer cells, 1,25,26 as well as in endometrial, 2,27 uterine cervix, 28 ovarian, 3 prolactinsecreting and plurihormonal pituitary adenomas, 29 and in non-small cell lung cancer. 30 Similar to our statement on normal meninges, to date, there are no data in the literature on aromatase expression in meningiomas, which demonstrated negative in the present series.…”

Section: Discussionmentioning

confidence: 96%

Immunohistochemical expression of aromatase and estrogen, androgen and progesterone receptors in normal and neoplastic human meningeal cells

et al. 2010

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Evidence suggests that sex hormones may play a role in the tumorigenesis of meningiomas, and studies have demonstrated the expression of hormone receptors in these tumors. Aromatase expression has been detected in several normal tissues, including neurons in the CNS, and tumor tissues. We aim to assess the expression of aromatase (ARO) and of progesterone receptor (PR), estrogen receptor (ER) and androgen receptor (AR) in both normal and neoplastic meningeal cells. A cross-sectional study was conducted with 126 patients diagnosed with meningioma (97 women and 29 men; mean age, 53.6 years) submitted to neurosurgery at Hospital São José, Complexo Hospitalar Santa Casa de Porto Alegre, southern Brazil. Control sections of normal meningeal cells, 19 patients, were obtained by evaluating the arachnoid tissue present in the arachnoid cyst resected material. Immunohistochemistry was applied to assess ARO, PR, ER and AR. Aromatase expression was detected in 100% of the control patients and in 0% of the patients with meningioma. ER was present in 24.6% of the meningiomas and in 0% of the controls, AR in 18.3% of the meningiomas and in 0% of the controls, and PR in 60.3% of the meningiomas and in 47.4% of the controls. A positive association was observed between the presence of AR and ER (OR 3.7; P = 0.01) in meningiomas. There were no significant differences in the presence of hormone receptors between meningioma histological subtypes. PR expression in women with meningioma was significantly higher than that found in men (OR 2.3; P = 0.08). Behavior pattern differences observed between aromatase expression, present in normal tissues and absent in meningiomas, and estrogen and androgen hormone receptors, absent in normal tissues and present in meningiomas, suggest that there is heterogeneity in modulation by sex steroids in the development of these tumors.

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Section: Discussionmentioning

confidence: 96%

Immunohistochemical expression of aromatase and estrogen, androgen and progesterone receptors in normal and neoplastic human meningeal cells

et al. 2010

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“…These tumors are often preceded by endometrial premalignant disease and are always estrogen nuclear receptor (ER) and progesterone receptor (PR)-positive, which frequently arise during excessive estrogen exposure. Recently, much effort has been made to confirm the involvement of aberrant estrogen metabolism in dysregulated endometrial cancer cell growth and malignant metastasis (4)(5)(6). We previously suggested that estrogen promoted endometrial cancer cell proliferation and invasion by fat mass and obesityassociated (FTO) gene (7), however, the molecular mechanism of how FTO regulates cellular growth by estrogen remains obscure.…”

Section: Introductionmentioning

confidence: 99%

Estrogen promotes fat mass and obesity-associated protein nuclear localization and enhances endometrial cancer cell proliferation via the mTOR signaling pathway

et al. 2016

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Extensive exposure to estrogen is generally acknowledged as a risk factor for endometrial cancer. Given that the accumulation of adipocytes also contributes to the increased production of estrogen, in the present study, we evaluated the expression of the fat mass and obesity-associated (FTO) gene in endometrial tumor tissues and further explored the mechanism of how estrogen facilitates FTO nuclear localization and promotes endometrial cancer cell proliferation. Immunohistochemical (IHC) staining assay was used to detect the FTO expression in endometrial tumor samples. Western blotting was performed to investigate the mechanism of estrogen-induced FTO nuclear localization. siRNA was used to knock down ERα and further explore its role in FTO nuclear localization. MTT assay was carried out to determine cell proliferation. We found that FTO was overexpressed in endometrial carcinoma tissues and served as a poor prognostic marker. Additionally, estrogen induced FTO nuclear accumulation via the mTOR signaling pathway and the nuclear localization was ERα-dependent, which contributed to enhanced proliferative activity. Therefore, the present study provides new insight into the mechanisms of estrogen-induced proliferation, implying the possibility of using FTO as a potential therapeutic target for the treatment of endometrial cancer.

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“…В настоящее время сформирована убедительная точка зрения в отношении возрастающего онкологического риска при мС. Признана роль инсулинорезистентности, системы инсулиноподобных факторов роста, адипокинов, секретируемых из висцеральных адипоцитов [5,26,27], свободных жирных кислот, локального эстрогенообразования и гиперандрогенизации [28,49] в создании предрасположенности к развитию ряда онкологических заболеваний, а также показано значение молекулярно-генетических факторов, часть из которых ассоциирована с гормонально-метаболическими нарушениями, как основы для формирования различных патогенетических вариантов опухолей. общность патогенетических механизмов развития мС и канцерогенеза позволяет определить дополнительные факторы риска возникновения ракового перерождения тканей, наметить возможные пути первичной немедикаментозной и, возможно, медикаментозной профилактики [25].…”

Section: актуальностьunclassified

Structural Features of the Metabolic Syndrome: Clinical and Epidemiological Aspects. Relationship With Proliferative Processes and Endometrial Cancer

Kishkina¹,

Коломиец²,

Yunusova³

2019

Problems in oncology

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This literature review is devoted to the relationship of the structural features of the metabolic syndrome in proliferative processes and endometrial cancer (EC), and the identification of the relationship between the individual components of the metabolic syndrome and the development of endometrial cancer. The metabolic syndrome is currently a global medical and social problem, which is due to the wide spread of this symptom complex in the population. Today, the main concept of this syndrome is the concept of a cluster of components associated with an increased risk of developing type 2 diabetes and cardiovascular diseases. It is known that an increase in the mass of adipose tissue above the norm by 20% or more leads to dysfunction of the hypothalamic-pituitary-ovarian system. At the same time, the risk of RE on the background of metabolic syndrome increases by 2-3 times. This probability also largely depends on the severity of proliferation in the endometrium, which is caused by the presence of dyshormonal and metabolic disorders. In addition, this is due to the aggravation of insulin resistance, an increase in the production of androgens by the ovaries, the formation of stable anovulation and, as a result, the progression of pathological changes in the endometrium. With the onset of peri - and postmenopausal endometrial hyperplasia in about 50% of cases progressing to malignant pathology. The role of the system of insulin-like growth factors, adipokines secreted from visceral adipocytes of free fatty acids, local estrogen formation and hyperandrogenization is also recognized in creating a predisposition to the EC formation. According to the results of the study of the functioning of the autocrine-paracrine system of adipose tissue, the risk of endometrial proliferative processes is higher at low levels of adiponectin and high levels of insulin. All this indicates the feasibility of monitoring the status of adipose tissue.

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Enzymes of estrogen metabolism in endometrial cancer

Cited by 8 publications

References 3 publications

Immunohistochemical expression of aromatase and estrogen, androgen and progesterone receptors in normal and neoplastic human meningeal cells

Immunohistochemical expression of aromatase and estrogen, androgen and progesterone receptors in normal and neoplastic human meningeal cells

Estrogen promotes fat mass and obesity-associated protein nuclear localization and enhances endometrial cancer cell proliferation via the mTOR signaling pathway

Structural Features of the Metabolic Syndrome: Clinical and Epidemiological Aspects. Relationship With Proliferative Processes and Endometrial Cancer

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