Interrelationship of Runx2 and estrogen pathway in skeletal tissues

Jeong, Jae Hwan; Choi, Je Yong

doi:10.5483/bmbrep.2011.44.10.613

Cited by 17 publications

(10 citation statements)

References 62 publications

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“…Exogenous addition of FGF4 significantly diminished DAG-induced increases in the mRNA levels of Runx2 and osterix, but not of OC and BSP. Runx2 and osterix are essential osteoblast-specific transcription factors regulating bone differentiation [42], [43]. These factors activate a repertoire of genes during differentiation of pre-osteoblasts into mature osteoblasts and osteocytes [42], [44].…”

Section: Discussionmentioning

confidence: 99%

“…Runx2 and osterix are essential osteoblast-specific transcription factors regulating bone differentiation [42], [43]. These factors activate a repertoire of genes during differentiation of pre-osteoblasts into mature osteoblasts and osteocytes [42], [44]. Osterix is also critical for differentiation of Runx2-expressing precursors into mature and functional osteoblasts, and expression of osterix mRNA and protein is positively regulated by Runx2 [43].…”

Section: Discussionmentioning

confidence: 99%

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Fibroblast Growth Factor-4 Enhances Proliferation of Mouse Embryonic Stem Cells via Activation of c-Jun Signaling

et al. 2013

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Fibroblast growth factor-4 (FGF4) is expressed in embryonic stages and in adult tissues, where it plays critical roles in modulating multiple cellular functions. However, the exact roles of FGF4 on proliferation and differentiation of embryonic stem cells (ESCs) are not completely understood. Exogenous addition of FGF4 stimulated proliferation of mouse ESCs (mESCs), as proven by the increases in DNA synthesis and cell cycle regulatory protein induction. These increases were almost completely inhibited by pre-treating cells with anti-FGF4 antibody. FGF4 also activated c-Jun N-terminal kinase (JNK) and extracellular-signal regulated kinase (ERK) signaling, but not p38 kinase. Blockage of JNK signaling by SP600125 or by transfection with its specific siRNA significantly inhibited FGF4-stimulated cell proliferation through the suppression of c-Jun induction and activator protein-1 (AP-1) activity. However, ERK or p38 kinase inhibitor did not affect FGF4-stimulated proliferation in mESCs. FGF4 suppressed osteogenic differentiation of mESCs by inhibiting expression of transcription factors involved in bone formation. Further, exogenous FGF4 addition stimulated proliferation of human periodontal ligament stem cells (hPDLSCs) and bone marrow mesenchymal stem cells (BMMSCs) via activation of ERK signaling. FGF4 also augmented mineralization of hPDLSCs, but not of BMMSCs. Collectively, it is suggested that FGF4 triggers proliferation of stem cells by activating MAPK-mediated signaling, while it affects differently osteogenic differentiation according to the origins of stem cells.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Fibroblast Growth Factor-4 Enhances Proliferation of Mouse Embryonic Stem Cells via Activation of c-Jun Signaling

et al. 2013

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“…The function of RUNX2 is related with several molecules and multiple pathways, such as angiogenic factor, matrix metalloproteinases (MMPs), transcription factors, the MAPK pathway, the STAT pathway and the PI3 K pathway [27], which are involved in ovarian carcinogenesis. For example, Duan et al [28] indicated that the abnormal activation on PI3 K/PKB signaling pathway may be correlated with the occurrence and development of EOC; Chakrabarty and Kondratick [29] also suggested that activation on multiple cascades of the MAPK pathway may promote the invasion and metastasis of EOC.…”

Section: Discussionmentioning

confidence: 99%

Overexpression of Runt-Related Transcription Factor-2 Is Associated with Advanced Tumor Progression and Poor Prognosis in Epithelial Ovarian Cancer

Lin

et al. 2012

Journal of Biomedicine and Biotechnology

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Aim. To investigate clinical significance of runt-related transcription factor (RUNX)-2 in epithelial ovarian cancer (EOC). Methods. RUNX2 protein expression and its subcellular localization were detected by immunohistochemistry in 116 patients with EOC. Results. RUNX2 protein was predominantly expressed in cell nucleus of EOC tissues. The expression level of RUNX2 in EOC tissues was significantly higher than that in normal ovarian tissues (P < 0.001). In addition, the nuclear labeling index (LI) of RUNX2 in tumor cells was significantly associated with the advanced clinical stage of EOC tissues (P = 0.001). Moreover, EOC patients with high RUNX2 LI had significantly shorter overall (P < 0.001) and progression-free (P = 0.002) survival than those with low RUNX2 LI. Especially, subgroup analysis revealed that EOC patients with high clinical stages (III~IV) in high RUNX2 expression group demonstrated a significantly worse clinical outcome than those in low RUNX2 expression group, but patients with low clinical stages (I~II) had no significantly different prognosis between high and low RUNX2 expression groups. Conclusions. Our data suggest for the first time that RUNX2 overexpression is associated with advanced tumor progression and poor clinical outcome of EOC patients. RUNX2 might be a novel prognostic marker of EOC.

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“…Although we cannot explain the mechanisms involved, it is postulated that irradiation at ＞2 Gy caused DNA damage and growth inhibition at early exposure times, which led to delayed recovery in cell cycle progression with the attendant stimulation of TGF-β1 expression even at 7 days post-irradiation in primary osteoblasts. Runx2, also known as core binding factor alpha 1, plays an essential role in osteoblast differentiation through transcriptional regulation of bone-specific genes (25)(26)(27)(28). A considerable number of findings suggest a relationship between TGF-β1 and Runx2 (29).…”

Section: Discussionmentioning

confidence: 99%

X-ray radiation at low doses stimulates differentiation and mineralization of mouse calvarial osteoblasts

Park¹,

Kim²,

Lee³

et al. 2012

BMB Reports

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Radiotherapy is considered to cause detrimental effects on bone tissue eventually increasing bone loss and fracture risk. However, there is a great controversy on the real effects of irradiation itself on osteoblasts, and the mechanisms by which irradiation affects osteoblast differentiation and mineralization are not completely understood. We explored how X-ray radiation influences differentiation and bone-specific gene expression in mouse calvarial osteoblasts. Irradiation at 2 Gy not only increased differentiation and mineralization of the cells, but also upregulated the expression of alkaline phosphatase, type I collagen, osteopontin, and osteocalcin at early stages of differentiation. However, irradiation at higher doses (＞2 Gy) did not stimulate osteoblast differentiation, rather it suppressed DNA synthesis by the cells without a toxic effect. Additional experiments suggested that transforming growth factor-beta 1 and runt-transcription factor 2 play important roles in irradiation-stimulated bone differentiation by acting as upstream regulators of bone-specific markers. [BMB Reports 2012; 45(10): 571-576]

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Interrelationship of Runx2 and estrogen pathway in skeletal tissues

Cited by 17 publications

References 62 publications

Fibroblast Growth Factor-4 Enhances Proliferation of Mouse Embryonic Stem Cells via Activation of c-Jun Signaling

Fibroblast Growth Factor-4 Enhances Proliferation of Mouse Embryonic Stem Cells via Activation of c-Jun Signaling

Overexpression of Runt-Related Transcription Factor-2 Is Associated with Advanced Tumor Progression and Poor Prognosis in Epithelial Ovarian Cancer

X-ray radiation at low doses stimulates differentiation and mineralization of mouse calvarial osteoblasts

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