Stanniocalcin-1 as a Novel Marker to Detect Minimal Residual Disease of Human Leukemia

Tohmiya, Yasuo; Koide, Yuji; Fujimaki, Shin; Harigae, Hideo; Funato, Tadao; Kaku, Mitsuo; Ishii, Tomonori; Munakata, Yasuhiko; Kameoka, Junichi; Sasaki, Takeshi

doi:10.1620/tjem.204.125

Cited by 29 publications

(33 citation statements)

References 22 publications

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“…Current evidences support the notion that STC1 is involved in human cancer development [Chang et al, 2003;Eisenhofer et al, 2004;McCudden et al, 2004;Tohmiya et al, 2004;Koide and Sasaki, 2006;Nakagawa et al, 2007;Joensuu et al, 2008;Macartney-Coxson et al, 2008;Klopfleisch and Gruber, 2009]. Our previous studies have revealed that, STC1 is a HIF-1 target gene and was epigenetic regulated by histone deacetylation [Yeung et al, 2005;Law et al, 2008Law et al, , 2010.…”

Section: Discussionsupporting

confidence: 75%

Sp1 is a transcription repressor to stanniocalcin-1 expression in TSA-treated human colon cancer cells, HT29

et al. 2011

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Our previous study demonstrated that, stanniocalcin-1 (STC1) was a target of histone deacetylase (HDAC) inhibitors and was involved in trichostatin A (TSA) induced apoptosis in the human colon cancer cells, HT29. In this study, we reported that the transcriptional factor, specificity protein 1 (Sp1) in association with retinoblastoma (Rb) repressed STC1 gene transcription in TSA-treated HT29 cells. Our data demonstrated that, a co-treatment of the cells with TSA and Sp1 inhibitor, mithramycin A (MTM) led to a marked synergistic induction of STC1 transcript levels, STC1 promoter (1 kb)-driven luciferase activity and an increase of apoptotic cell population. The knockdown of Sp1 gene expression in TSA treated cells, revealed the repressor role of Sp1 in STC1 transcription. Using a protein phosphatase inhibitor okadaic acid (OKA), an increase of Sp1 hyperphosphorylation and so a reduction of its transcriptional activity, led to a significant induction of STC1 gene expression. Chromatin immunoprecipitation (ChIP) assay revealed that Sp1 binding on STC1 proximal promoter in TSA treated cells. The binding of Sp1 to STC1 promoter was abolished by the co-treatment of MTM or OKA in TSA-treated cells. Re-ChIP assay illustrated that Sp1-mediated inhibition of STC1 transcription was associated with the recruitment of another repressor molecule, Rb. Collectively our findings identify STC1 is a downstream target of Sp1.

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Section: Discussionsupporting

confidence: 75%

Sp1 is a transcription repressor to stanniocalcin-1 expression in TSA-treated human colon cancer cells, HT29

et al. 2011

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“…In addition, the STC-1 mRNA expression in blood is closely related to tumor size in breast cancer, micrometastases of hepatocellular carcinoma, and minimal residual disease in leukemia. 39 Very recently, stanniocalcins (STC-1 and STC-2) were shown to be expressed in breast cancers of lower grade with a slow initial progression of the tumor and to act as a survival factor contributing to the extended survival or dormancy of micrometastases with a cumulative risk for late relapses. 40 Another biomarker candidate presently identified is periostin.…”

Section: Discussionmentioning

confidence: 99%

Entering a New Era of Rational Biomarker Discovery for Early Detection of Melanoma Metastases: Secretome Analysis of Associated Stroma Cells

et al. 2009

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Metastasis in melanoma is associated with poor prognosis. Early detection may thus substantially improve patient survival. Here we present a novel biomarker discovery strategy based on proteome profiling and secretome analysis of primary cells. Tumor associated stroma cells secrete proteins that may act as powerful tumor promoters. This cell cooperativity is reversible and may thus be directly accessible to therapeutic intervention. The onset of these characteristic events seems to precede tumor progression. Thus, proteins specifically secreted by these cells may serve as early disease biomarkers. Due to the leaky nature of newly formed blood vessels and the increased hydrostatic pressure within tumors, secreted proteins are most plausibly shed into the blood. Our analysis strategy is based on three different model systems, including established cultured cell lines, animal model systems, and clinical human samples. The feasibility is demonstrated with secretome and proteome profiles generated from normal human skin fibroblasts in comparison to melanoma-associated fibroblasts isolated from mouse xenografts and fibroblasts from bone marrow of multiple myeloma patients. Further mutual comparisons were enabled including proteome profiles of melanocytes and M24met melanoma cells. All shotgun proteomics data are accessible via the PRIDE database. Among others, the candidate biomarkers GPX5, secreted by melanoma cells, in addition to periostin and stanniocalcin-1, which are expressed by melanoma-associated fibroblasts were identified. In conclusion, this is a novel strategy to identify diagnostic marker proteins aiding early detection of metastatic melanoma and to improve our understanding of pathomechanisms involving the microenvironment to enable the design of novel therapeutic strategies.

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“…ABCA1 deficiency is associated with the Scott syndrome, a bleeding disorder characterized by a failure to expose phosphatidylserine on the outer leaflet of the platelet plasma membrane [53]. Another underexpressed gene, STC1 (stanniocalcin 1) was directly correlated to acute leukemia at diagnosis and relapse [54]. The tumor necrosis factor, alpha-induced protein 6 gene (TNFAIP6) was underexpressed in isoflavone-treated subjects.…”

Section: Discussionmentioning

confidence: 99%

Dietary isoflavones differentially induce gene expression changes in lymphocytes from postmenopausal women who form equol as compared with those who do not

Niculescu

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Fischer

et al. 2007

The Journal of Nutritional Biochemistry

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Human and animal studies suggest that dietary soy isoflavones reduce cancer risk, ameliorate postmenopausal syndrome and decrease bone resorption in postmenopausal women. The capacity to form the metabolite equol from daidzein is suggested as an important modulator of response to isoflavones; this capacity depends on gut colonization with appropriate bacteria. We administered a dietary supplement containing high-dose purified soy isoflavones (genistein, 558 mg/day; daidzein, 296 mg/day; and glycitein, 44 mg/day) to 30 postmenopausal women for 84 days and collected peripheral lymphocytes at timed intervals. Using microarray analysis, we determined whether changes in gene expression associated with this treatment support existing hypotheses as to isoflavones' mechanisms of action. Expression of a large number of genes was altered by isoflavone treatment, including induction of genes associated with cyclic adenosine 3′,5′-monophosphate (cAMP) signaling and cell differentiation and decreased expression of genes associated with cyclindependent kinase activity and cell division. We report that isoflavone treatment in subjects who have the capacity to produce equol differentially affects gene expression as compared with nonproducers, supporting the plausibility of the importance of equol production. In general, isoflavones had a stronger effect on some putative estrogen-responsive genes in equol producers than in nonproducers. Our study suggests that, in humans, isoflavone changes are related to increased cell differentiation, increased cAMP signaling and G-protein-coupled protein metabolism and increased steroid hormone receptor activity and have some estrogen agonist effects; equol-production status is likely to be an important modulator of responses to isoflavones.

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Stanniocalcin-1 as a Novel Marker to Detect Minimal Residual Disease of Human Leukemia

Cited by 29 publications

References 22 publications

Sp1 is a transcription repressor to stanniocalcin-1 expression in TSA-treated human colon cancer cells, HT29

Sp1 is a transcription repressor to stanniocalcin-1 expression in TSA-treated human colon cancer cells, HT29

Entering a New Era of Rational Biomarker Discovery for Early Detection of Melanoma Metastases: Secretome Analysis of Associated Stroma Cells

Dietary isoflavones differentially induce gene expression changes in lymphocytes from postmenopausal women who form equol as compared with those who do not

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