Evolution and roles of stanniocalcin

Yeung, Bonnie H. Y.; Law, Alice Y.S.; Wong, Chris K C

doi:10.1016/j.mce.2011.11.007

Cited by 190 publications

(194 citation statements)

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“…Also, the involvement of PAPP-A in cancer development is increasingly recognized (32), and is underscored by the finding that PAPP-A knock-out mice have a remarkably low incidence of spontaneous age-related tumors (22). It is therefore interesting that multiple reports link both stanniocalcins to human cancers, although both up-and down-regulations have been reported (24,26). For example, loss of BRCA1 tumor suppressor function in breast cancer causes STC1 expression to become undetectable (54), and late relapse of breast cancer correlates with high expression of STC1 and STC2 (55).…”

Section: Discussionmentioning

confidence: 99%

Stanniocalcin-2 Inhibits Mammalian Growth by Proteolytic Inhibition of the Insulin-like Growth Factor Axis

Jepsen¹,

Kløverpris²,

Mikkelsen³

et al. 2015

Journal of Biological Chemistry

124

125

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Background:The biological function and biochemical activity of mammalian stanniocalcin-2 are unknown. Results: Stanniocalcin-2 inhibits proteolytic release of insulin-like growth factor (IGF), and its ability to cause growth retardation upon transgenic overexpression in mice depends on its proteinase inhibitory function. Conclusion: Stanniocalcin-2 is a novel component of the IGF axis. Significance: Altered stanniocalcin-2 expression may affect IGF signaling under pathological conditions.

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Section: Discussionmentioning

confidence: 99%

Stanniocalcin-2 Inhibits Mammalian Growth by Proteolytic Inhibition of the Insulin-like Growth Factor Axis

Jepsen¹,

Kløverpris²,

Mikkelsen³

et al. 2015

Journal of Biological Chemistry

124

125

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“…Current evidence illustrates the differential expression patterns of STC1 in paired tumor and normal tissues (Liu et al 2010, Tamura et al 2011. A role of STC1 in the tumor microenvironment has also been suggested (Yeung et al 2012). This presumption is strengthened by the involvement of STC1 in local inflammation (Sheikh--Hamad 2010) as well as the identification of STC1 as a hypoxia and angiogenic responsive gene (Yeung et al 2005, Law et al 2010, Jauhiainen et al 2011, Roch & Sherwood 2011.…”

Section: Discussionmentioning

confidence: 99%

“…This inconsistency may not be contradictory as the transcriptional factor, NF-kB, is also known to be able to protect or contribute to apoptosis (Foo & Nolan 1999, Fan et al 2008. Therefore, STC1 may not be a key regulator for or against apoptosis; the particular role of STC1 is probably dependent on the extent of cellular stress imposed to the cells (Yeung et al 2012).…”

Section: Discussionmentioning

confidence: 99%

“…Different from piscine, mammalian STC1 is expressed in a wide variety of tissues, acting on its target cells via autocrine/paracrine pathways (Varghese et al 1998, De Niu et al 2000. Therefore, the site of synthesis and release as well as the mode of action of mammalian STC1 may be altered during evolution (Yeung et al 2012). This alternation might lead to the change in the physiological functions of STC1 from the regulation of whole-body Ca 2C /P i homeostasis in fish to signaling at cellular and tissue levels in mammals.…”

Section: Introductionmentioning

confidence: 99%

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Synergistic effect of p53 on TSA-induced stanniocalcin 1 expression in human nasopharyngeal carcinoma cells, CNE2

Ching

Yeung

Wong³

2012

Journal of Molecular Endocrinology

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Human stanniocalcin 1 (STC1) has recently been identified as a putative protein factor involved in cellular apoptosis. The use of histone deacetylase inhibitor (i.e. trichostatin A (TSA)) and doxorubicin (Dox) is one of the common treatment methods to induce apoptosis in human cancer cells. A study on TSA and Dox-mediated apoptosis may shed light on the regulation and function of STC1 in cancer treatment. In this study, TSA and Dox cotreatment in human nasopharyngeal carcinoma cells (CNE2) elicited synergistic effects on STC1 gene expression and cellular apoptosis. An activation of p53 (TP53) transcriptional activity in Dox-or DoxCTSA-treated cells was revealed by the increased expression levels of p53 mRNA/protein as well as p53-driven luciferase activities. To elucidate the possible involvement of p53 in STC1 gene transcription, a vector expressing wild-type or dominant negative (DN) p53 was transiently transfected into the cells. Both STC1 promoter luciferase constructs and chromatin immunoprecipitation assays did not support the direct role of p53 in STC1 gene transactivation. However, the synergistic effects of p53 on the induction of NF-kB phosphorylation and the recruitment of acetylated histone H3 in STC1 promoter were observed in TSA-cotreated cells. The overexpression of exogenous STC1 sensitized apoptosis in Dox-treated cells. Taken together, this study provides data to show the cross talk of NF-kB, p53, and histone protein in the regulation of STC1 expression and function.

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“…STC1 was originally discovered in mammals and in the endocrine glands of the kidneys, and stannius corpuscles of bony fishes (21). STC1 is expressed in a wide variety of tissues, such as the heart, prostate, adrenal gland, lung, kidney, liver and thyroid gland (22)(23)(24). Multiple lines of evidence show that mammalian STC1 was cloned as a cancer-related gene (25).…”

Section: Introductionmentioning

confidence: 99%

Klotho inhibits human follicular thyroid cancer cell growth and promotes apoptosis through regulation of the expression of stanniocalcin-1

Dong

Wang

et al. 2015

Oncology Reports

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Abstract.The new anti-aging gene Klotho has been identified as a multi-functional humoral factor which influences multiple biological processes, including tumor progression. Although ample evidence indicates that Klotho plays important roles in cervical, lung and breast cancer, the role and mechanism of Klotho in thyroid cancer are still unclear. The present study aimed to investigate the effects and mechanisms of Klotho in human thyroid cancer cell lines FTC133 and FTC238. Klotho overexpression markedly reduced thyroid cancer FTC133 and FTC238 cell proliferation and enhanced apoptosis, whereas, Klotho silencing in the FTC133 and FTC238 cells increased cell growth. Moreover, soluble human KL1 (sKL) and Klotho overexpression had a similar effect on FTC133 and FTC238 cell growth. A high level of Klotho was also found to be associated with a low level of stanniocalcin 1 (STC1) in both the FTC133 and FTC238 cell lines. STC1 silencing significantly inhibited thyroid cancer cell proliferation, whereas recombinant human STC1 (hSTC1) markedly enhanced cell proliferation. In addition, our study demonstrated that hSTC1 treatment attenuated Klotho-induced inhibition of cell proliferation and promotion of apoptosis. Our data revealed the existence of a moderating effect between Klotho and STC1, where Klotho may inhibit thyroid tumor progression by inhibiting the tumor marker level of STC1. IntroductionThyroid cancer is the most common endocrine malignancy, and the number of new cases diagnosed worldwide has increased in the last decade (1). Thyroid cancer is classified into undifferentiated and differentiated cancer, and the vast majority of thyroid cancers (~80%) are differentiated thyroid cancers (DTCs) (2). DTCs consist of two cellular types: papillary thyroid cancers (PTCs) and differentiated follicular thyroid cancers (FTCs). Various effective treatments have been used for thyroid cancer therapy, such as complete thyroidectomy followed by radioiodine therapy (3). These patients have a low mortality rate and excellent prognosis. However, a subset of patients that develops distant metastases presents with a high disease recurrence rate and poor prognosis and the disease may develop into anaplastic thyroid cancer with a fatal outcome (4,5). Therefore, research on the molecular mechanisms involved in thyroid carcinogenesis will facilitate the development of more effective therapy for this cancer.Ample evidence indicates that aging is the main risk factor for cancer, and most cancers are diagnosed in individuals over 55 years of age (6). Currently, Klotho has recently been identified as a new anti-aging gene and has gained much attention (7). Klotho (KL), a 1012-amino acid type I single-pass transmembrane protein, is widely expressed in various types of tissues, such as brain, kidney, various exocrine and endocrine tissues, including the thyroid gland (8-10). The Klotho gene is composed of 5 exons (8,11) and contains an intracellular domain and an extracellular domain. The extracellular domain of Klotho is composed of two d...

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Evolution and roles of stanniocalcin

Cited by 190 publications

References 149 publications

Stanniocalcin-2 Inhibits Mammalian Growth by Proteolytic Inhibition of the Insulin-like Growth Factor Axis

Stanniocalcin-2 Inhibits Mammalian Growth by Proteolytic Inhibition of the Insulin-like Growth Factor Axis

Synergistic effect of p53 on TSA-induced stanniocalcin 1 expression in human nasopharyngeal carcinoma cells, CNE2

Klotho inhibits human follicular thyroid cancer cell growth and promotes apoptosis through regulation of the expression of stanniocalcin-1

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