Comparative study of glycoconjugates of the rat prostatic lobes by lectin histochemistry

Chan, Franky L.; Ho, Shuk‐Mei

doi:10.1002/(sici)1097-0045(19990101)38:1<1::aid-pros1>3.0.co;2-6

Cited by 23 publications

(17 citation statements)

References 59 publications

(83 reference statements)

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“…TGFα/EGF receptor signaling; 41 TGFβ signaling, 42 IGF-1 and VEGF signaling, 43 and ER signaling); 44 c) prolactinemia or increased prolactin-receptor signaling; 45 d) mitogen-activated protein kinase (MAPK) activation, possibly through Id-1; 46;47 e) increased cell-survival potential through the overexpression of anti-apoptotic mediators (e.g., metallothionein 48 and TRPM-2/clusterin); 49;50 f) elevation in oxidative stress-induced DNA damage; 51-53 g) changes in gene-expression profiles related to cell proliferation, DNA damage, activation of proto-oncogenes and transforming factors, IL-1B signaling, and TNF-α activation; 54;55 and h) breakdown of epithelial basement membrane and stromal extracellular matrix due to the increase in gelatinolytic proteinase activity and altered expression of glycoconjugates in smooth muscles and their associated extracellular matrix. 56-58 Another potential culprit associated with estrogen-induced/promoted PCa is hormone-induced chronic inflammation, 38;59-61 although this view is not uniformly supported by all studies. 62 …”

Section: Epidemiologic and Animal-model Studies Of The Relationship Bmentioning

confidence: 99%

Estrogens and Prostate Cancer: Etiology, Mediators, Prevention, and Management

Lee

Lam

et al. 2011

Endocrinology and Metabolism Clinics of North America

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The relationship between hormones and the pathogenesis of prostate cancer (PCa) has been studied extensively. All the mainstay targets for hormonal PCa therapies are based on negating androgen action. Recent epidemiologic and experimental data have clearly pinpointed the key roles of estrogens in PCa development and progression. Racial and geographical differences, as well as age-associated changes, in estrogen synthesis and metabolism contribute significantly to the etiology by increasing the ratio of circulating estrogen to androgen, sex hormone binding globulin synthesis, and aromatase activity and reducing androgen glucuronidation and tissue bioactivation. Promotion of aberrant cell growth, evasion of apoptosis, increased oxidative stress and inflammation, and gains in adiposity and bioactivation to genotoxic carcinogens during adulthood are probable mechanisms of estrogen carcinogenicity, while “estrogen imprinting” via epigenetics in early-life also determines PCa risk. Although the effects of estrogens are known to be mediated by genomic actions of the two estrogen receptor (ER) subtypes (ERα and ERβ), other non-canonical mediators, including the different ERβ isoforms, membrane and mitochondrial ERs, and G protein-coupled receptor 30, may have major actions diverging from classical ER actions. These new discoveries have led to renewed interest among the public and the medicinal field in estrogens and antiestrogens as singular and adjuvant PCa treatment and prevention regimens. This review summarizes current knowledge on how different estrogens/antiestrogens/estrogen mimics contribute to prostate carcinogenesis, the roles of the different mediators of estrogen in the process, and the potentials of new estrogenic/antiestrogenic compounds as targeted therapies for prevention and treatment of PCa.

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Section: Epidemiologic and Animal-model Studies Of The Relationship Bmentioning

confidence: 99%

Estrogens and Prostate Cancer: Etiology, Mediators, Prevention, and Management

Lee

Lam

et al. 2011

Endocrinology and Metabolism Clinics of North America

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“…Thus, such a voluminous proportion of secretory substances suggests that glycoconjugates may have great implications for the physiological activity of spermatozoa. Glycohistochemical studies on the epithelial cells of the prostate gland have previously been performed in the rat [8,33], guinea pig [9], goat [34], pig [35], rhesus monkey [40], and human [1,5], and the results obtained in these studies have shown that secretory glycoconjugates are unusually important constituents in view of the histophysiological functions of the sex glands.…”

Section: Introductionmentioning

confidence: 99%

Histochemical Analysis of Glycoconjugates in the Disseminate Prostate Gland of the Wild Boar (Sus scrofa riukiuanus)

Sakairi

Tsukise

Nara

et al. 2003

Acta Histochem. Cytochem

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The results obtained in the present study demonstrated the precise localization and characterization of glycoconjugates in the disseminate prostate gland of the wild boar, using glycohistochemical methods including lectin techniques in light microscopy. According to the present results, it was apparent that glycoconjugates with neutral and acidic groupings were contained in the secretory epithelial cells and luminal secretions. In these glycoconjugates, a series of saccharide residues were visualized such as a-D-glucose, a-D-mannose, a-Lfucose, b-D-galactose, N-acetyl-D-galactosamine, N-acetyl-D-glucosamine, and N-acetyl-neuraminic acid (sialic acid). In addition, an abundance of glycoconjugates with terminal sialic acids was revealed in the peripheral parts of the prostate gland, as compared with its central parts. The terminal saccharide residues of glycoconjugates were more abundant in Siaa2-6Gal/GalNAc than those in Siaa2-3Galb1-4GlcNAc. Furthermore, some specifically MAA reactive acinous cells were detected in the glandular epithelium. The present histochemical results provide useful information regarding the close correlation between the physiological role of the disseminate prostate gland and the glandular glycoconjugates in the wild boar.

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“…Lectin histochemical studies demonstrated that lectins are useful as biomarkers of specific secretory functions, structural components and alterations of cells and tissues (Chan and Ho, 1999).…”

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confidence: 99%