Assessment of Stanniocalcin-1 mRNA as a molecular marker for micrometastases of various human cancers.

Fujiwara, Yoshiyuki; Sugita, Yurika; Nakamori, Shoji; Miyamoto, Atsushi; Shiozaki, Ken; Nagano, Hiroaki; Sakon, Masato; Monden, Morito

doi:10.3892/ijo.16.4.799

Cited by 42 publications

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“…Recently, STC1 has also been reported to be induced in a variety of tumors including the breast (McCudden et al, 2004), colon (Gerritsen et al, 2002), ovary (Ismail et al, 2000), lung cancer (Garber et al, 2001), thyroid medullary carcinoma (Watanabe et al, 2002), hepatocarcinoma (Okabe et al, 2001), pheochromocytoma (Eisenhofer et al, 2004), neuroblastoma (Wong et al, 2002), osteosarcoma and fibrosarcoma (Jellinek et al, 2000). The possible use of STC1 expression levels for the diagnosis of human breast, hepatocellular and colorectal cancer has also been proposed (Fujiwara et al, 2000;Wascher et al, 2003). Moreover, it has been shown that the inherited mutations of the RET gene, responsible for the MEN2A and MEN2B, are able to induce STC1 expression (Watanabe et al, 2002).…”

Section: Discussionmentioning

confidence: 99%

“…The STC1 gene is expressed in a wide variety of tissues, including the kidney, prostate, thyroid, bone and ovary (Chang et al, 1995;Olsen et al, 1996;Varghese et al, 1998). Recently, STC1 overexpression has been found in hepatocellular, colorectal, breast and medullary thyroid carcinomas (Fujiwara et al, 2000;Okabe et al, 2001;Watanabe et al, 2002;McCudden et al, 2004). Three sites in the 3 0 -UTR of ATXN1 gene and three in the 3 0 -UTR of STC1 gene, that match the miR-101b 'seed sequence', were predicted ( Figure 4a).…”

Section: Atxn1 and Stc1 Are Targets Of Mir-101bmentioning

confidence: 99%

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Regulation of microRNA expression by HMGA1 proteins

et al. 2009

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The High Mobility Group proteins HMGA1 are nuclear architectural factors that play a critical role in a wide range of biological processes. Since recent studies have identified the microRNAs (miRNAs) as important regulators of gene expression, modulating critical cellular functions such as proliferation, apoptosis and differentiation, the aim of our work was to identify the miRNAs that are physiologically regulated by HMGA1 proteins. To this purpose, we have analysed the miRNA expression profile of mouse embryonic fibroblasts (MEFs) carrying two, one or no Hmga1 functional alleles using a microarray (miRNA microarray). By this approach, we found a miRNA expression profile that differentiates Hmga1-null MEFs from the wild-type ones. In particular, a significant decrease in miR-196a-2, miR-101b, miR-331 and miR-29a was detected in homozygous Hmga1-knockout MEFs in comparison with wild-type cells. Consistently, these miRNAs are downregulated in most of the analysed tissues of Hmga1-null mice in comparison with the wild-type mice. ChIP assay shows that HMGA1 is able to bind regions upstream of these miRNAs. Moreover, we identified the HMGA2 gene product as a putative target of miR-196a-2, suggesting that HMGA1 proteins are able to downregulate the expression of the other member of the HMGA family through the regulation of the miR-196a-2 expression. Finally, ATXN1 and STC1 gene products have been identified as targets of miR-101b. Therefore, it is reasonable to hypothesize that HMGA1 proteins are involved in several functions by regulating miRNA expression.

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Section: Discussionmentioning

confidence: 99%

Section: Atxn1 and Stc1 Are Targets Of Mir-101bmentioning

confidence: 99%

Regulation of microRNA expression by HMGA1 proteins

et al. 2009

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“…A number of studies, mostly correlative, of mammalian STC1 mRNA and protein expression have ascribed roles to STC1 ranging from angiogenesis (Kahn et al, 2000;Bell et al, 2001), bone and muscle development (Jiang et al, 2000;Filvaroff et al, 2002;Varghese et al, 2002;Yoshiko et al, 2003), inflammation (Iyer et al, 1999;Kanellis et al, 2003), cellular metabolism (McCudden et al, 2002;Ellard et al, 2007) and cancer (Fujiwara et al, 2000;Ismail et al, 2000;Okabe et al, 2001;Welcsh et al, 2002). Establishing the functional importance and relevance of these putative functions has proved difficult; moreover, STC1-null mice housed in standard laboratory conditions have no obvious phenotype (Chang et al, 2005).…”

Section: Introductionmentioning

confidence: 99%

Stanniocalcin-1 acts in a negative feedback loop in the prosurvival ERK1/2 signaling pathway during oxidative stress

2009

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Mammalian Stanniocalcin-1 (STC1) is a glycoprotein that has been implicated in various biological processes including angiogenesis. Aberrant STC1 expression has been reported in breast, ovarian and prostate cancers, but the significance of this is not well understood. Here, we report that oxidative stress caused a 40-fold increase in STC1 levels in mouse embryo fibroblasts (MEFs). STC1À/À MEFs were resistant to growth inhibition and cell death induced by H 2 O 2 or by 20% O 2 (which is hyperoxic for most mammalian cells); this is the first phenotype reported for STC1-null cells. STC1À/À cells had higher levels of activated MEK and ERK1/2 than their wild-type (WT) counterparts, and these levels were all reduced by stable expression of exogenous STC1 in STC1À/À cells. Furthermore, pharmacological inhibition by PD98059 or UO126 of MEK and therefore of ERK1/2 activation restored sensitivity of STC1À/À cells to oxidative stress. We also found that H 2 O 2 -induced STC1 expression in WT cells was abolished by inhibition of ERK1/2 activation. Thus, the ERK1/2 signaling pathway upregulates STC1 expression, which in turn downregulates the level of activated MEK and consequently ERK1/2 in a novel negative feedback loop. Therefore, STC1 expression downregulates prosurvival ERK1/2 signaling and reduces survival under conditions of oxidative stress.

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“…Klotho inhibits STC1 expression in thyroid cancer cells. STC1 is a secreted glycoprotein hormone and a molecular marker for micrometastases of various human cancers, including thyroid cancer (27). yahata et al showed that the Klotho gene regulates the expression of STC1 and STC2 in the kidney (19).…”

Section: Loss Of Klotho Increases Human Cancer Cell Growth and Inhibimentioning

confidence: 99%

“…Multiple lines of evidence show that mammalian STC1 was cloned as a cancer-related gene (25). growing evidence suggests that STC1 expression may play an important role in human cancers, and high STC1 gene expression has been found in colorectal, breast, hepatocellular, carcinomas and thyroid cancers (26)(27)(28)(29). In the present study, we investigated whether Klotho expression is associated with the development of thyroid cancer via regulation of STC1 protein expression.…”

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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Assessment of Stanniocalcin-1 mRNA as a molecular marker for micrometastases of various human cancers.

Cited by 42 publications

References 0 publications

Regulation of microRNA expression by HMGA1 proteins

Regulation of microRNA expression by HMGA1 proteins

Stanniocalcin-1 acts in a negative feedback loop in the prosurvival ERK1/2 signaling pathway during oxidative stress

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

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