Runx2 Isoform I Controls a Panel of Proinvasive Genes Driving Aggressiveness of Papillary Thyroid Carcinomas

Sancisi, Valentina; Borettini, Gloria; Maramotti, Sally; Ragazzi, Moira; Tamagnini, Ione; Nicoli, Davide; Piana, Simonetta; Ciarrocchi, Alessia

doi:10.1210/jc.2012-1903

Cited by 45 publications

(58 citation statements)

References 40 publications

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“…Next, we tested the effect of TSA on RUNX2 promoter activity. We previously have shown that isoform I is the major RUNX2 isoform expressed in thyroid cancer patients (16). RT-PCR analysis confirmed that isoform II was not detectable in either TPC1 or BCPAP untreated cells and that TSA did not affect its expression.…”

Section: Hdaci Inhibit Runx2 Expression In Thyroid Cancer Cell Linesmentioning

confidence: 74%

“…Indeed, evidence exists that the use of the two promoters is context dependent. In particular, our group and others have shown that RUNX2 isoform I is the major RUNX2 isoform in tumor cells, while isoform II seems to be restricted to skeletal cells (16,26). Noticeably, the majority of molecular signals known to control RUNX2 act through the P1 promoter, while the regulation of the P2 promoter remains largely unknown (28)(29)(30).…”

Section: Introductionmentioning

confidence: 92%

“…Western blot analysis was performed as previously described (16). Antibodies used were goat anti-RUNX2 (AF2006; R&D Systems), rabbit anti-c-JUN (H-79, sc-1694; Santa Cruz Biotechnology, DBA Italia), mouse anti-actin (AC-15; Sigma-Aldrich), horseradish peroxidase-conjugated anti-goat (sc-2350; Santa Cruz Biotechnology), anti-rabbit and anti-mouse (GE Healthcare).…”

Section: Western Blot Analysismentioning

confidence: 99%

“…Factors that are crucial during embryogenesis are often hijacked during cancer progression, and RUNX2 is not an exception. RUNX2 is increasingly recognized in cancer biology for its oncogenic properties and a large number of articles link the deregulation of RUNX2 expression with progression and metastasization of different types of epithelial tumors (1,(3)(4)(5)(6)(7)(8)(9)(10)(11)(12)(13)(14)(15)(16)(17)(18). Regulation of RUNX2 may occur at multiple levels and through multiple signaling pathways.…”

Section: Introductionmentioning

confidence: 99%

“…However, the mechanisms that regulate the reactivation of this factor in cancer are still unknown. It has been reported that RUNX2 expression is higher in tumor than in normal tissue and that the level of expression of this protein has a negative prognostic value in a number of cancer types (16,(19)(20)(21)(22). The RUNX2 gene encodes for two isoforms starting from two separate promoters: the proximal P2 promoter expresses RUNX2 isoform I and the distal P1 promoter expresses isoform II (23,24).…”

Section: Introductionmentioning

confidence: 99%

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Histone Deacetylase Inhibitors Repress Tumoral Expression of the Proinvasive Factor RUNX2

Sancisi¹,

Gandolfi²,

Ambrosetti

et al. 2015

Cancer Research

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Aberrant reactivation of embryonic pathways occurs commonly in cancer. The transcription factor RUNX2 plays a fundamental role during embryogenesis and is aberrantly reactivated during progression and metastasization of different types of human tumors. In this study, we attempted to dissect the molecular mechanisms governing RUNX2 expression and its aberrant reactivation. We identified a new regulatory enhancer element, located within the RUNX2 gene, which is responsible for the activation of the RUNX2 promoter and for the regulation of its expression in cancer cells. Furthermore, we have shown that treatment with the anticancer compounds histone deacetylase inhibitor (HDACi) results in a profound inhibition of RUNX2 expression, which is determined by the disruption of the transcription-activating complex on the identified enhancer. These data envisage a possible targeting strategy to counteract the oncongenic function of RUNX2 in cancer cells and provide evidence that the cytotoxic activity of HDACi in cancer is not only dependent on the reactivation of silenced oncosuppressors but also on the repression of oncogenic factors that are necessary for survival and progression.Cancer Res; 75(9); 1868-82. Ó2015 AACR.

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Section: Hdaci Inhibit Runx2 Expression In Thyroid Cancer Cell Linesmentioning

confidence: 74%

Section: Introductionmentioning

confidence: 92%

Section: Western Blot Analysismentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 3 more Smart Citations

Histone Deacetylase Inhibitors Repress Tumoral Expression of the Proinvasive Factor RUNX2

Sancisi¹,

Gandolfi²,

Ambrosetti

et al. 2015

Cancer Research

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A multimodal integrative approach to model transcriptional addiction of thyroid cancer on RUNX2

Vitale

Sauta

Gugnoni

et al. 2022

Cancer Communications

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RUNX2 interacts with SCD1 and activates Wnt/β‐catenin signaling pathway to promote the progression of clear cell renal cell carcinoma

Song

Liu

et al. 2022

Cancer Medicine

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Background: Previous studies have demonstrated that Runt-associated transcription factor 2 (RUNX2) serves as the main transcription factor for osteoblast differentiation and chondrocyte maturation. RUNX2 is related to a variety of tumors, particularly tumor invasion and metastasis, while the expression and molecular mechanisms of RUNX2 in clear cell renal cell carcinoma (ccRCC) keep to be determined. Stearyl CoA desaturase 1 (SCD1), an endoplasmic reticulum fatty acid desaturase, transfers saturated fatty acids to monounsaturated fatty acids, is expressed highly in numerous malignancies. Methods:The Cancer Genome Atlas (TCGA) datebase and Western blot was used to analyzed the mRNA and protein levels of the target gene in ccRCC tissues and adjacent tissues. The proliferation ability of ccRCC cells was tested by colony forming and EdU assay. The migration ability of cells was detected by transwell assay. Immunoprecipitation was utilized to detect protein-protein interaction.Cycloheximide chase assay was used to measure the half-life of SCD1 protein. Results:In this study, the expressions of RUNX2 and SCD1 are increased in ccRCC tissues as well as ccRCC cell lines. Both RUNX2 and SCD1 could promote proliferation and migration in ccRCC cells. Furthermore, RUNX2 could physically interact with SCD1. In addition, the functional degradation and the inactivation of Wnt/β-catenin signaling pathway triggered by the downregulation of RUNX2 could be partly offset by the overexpression of SCD1. Conclusion:The findings indicate that the RUNX2/SCD1 axis may act as a potential therapeutic target via the Wnt/β-catenin signaling pathway of ccRCC. K E Y W O R D Sclear cell renal cell carcinoma, progression, runt-related transcription factor 2, stearyl CoA desaturase 1, Wnt/β-catenin Funding informationNo particular grant that belonged to funding agencies in public, commercial, or nonprofit fields was given to such a study.

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Runx2 Isoform I Controls a Panel of Proinvasive Genes Driving Aggressiveness of Papillary Thyroid Carcinomas

Cited by 45 publications

References 40 publications

Histone Deacetylase Inhibitors Repress Tumoral Expression of the Proinvasive Factor RUNX2

Histone Deacetylase Inhibitors Repress Tumoral Expression of the Proinvasive Factor RUNX2

A multimodal integrative approach to model transcriptional addiction of thyroid cancer on RUNX2

RUNX2 interacts with SCD1 and activates Wnt/β‐catenin signaling pathway to promote the progression of clear cell renal cell carcinoma

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