Mitotic Inheritance of mRNA Facilitates Translational Activation of the Osteogenic-Lineage Commitment Factor Runx2 in Progeny of Osteoblastic Cells

Varela, Nelson; Aránguiz, Alejandra; Lizama, Carlos O.; Sepúlveda, Hugo; Antonelli, Marcelo; Thaler, Roman; Moreno, Ricardo D.; Montecino, Martín; Stein, Gary S.; Wijnen, André J. van; Galindo, Mario

doi:10.1002/jcp.25188

Cited by 19 publications

(12 citation statements)

References 87 publications

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“…Gene expression analyses were performed using semi‐quantitative PCR as described previously [Varela et al, ] as a reproducible method that permits direct visualization of amplified cDNAs. Quantitation of mRNA expression detected by PCR was subsequently validated with next generation RNA sequencing (RNA‐seq) data that were concurrently generated for SAOS, MG63 and U2OS cell lines using procedures we previously described [Dudakovic et al, ].…”

Section: Methodsmentioning

confidence: 99%

Wnt/β‐Catenin Signaling Activates Expression of the Bone‐Related Transcription Factor RUNX2 in Select Human Osteosarcoma Cell Types

Vega

Lucero

Araya

et al. 2017

J of Cellular Biochemistry

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Osteosarcoma is the most common malignant bone tumor in children and adolescents. Metastasis and poor responsiveness to chemotherapy in osteosarcoma correlates with over-expression of the runt-related transcription factor RUNX2, which normally plays a key role in osteogenic lineage commitment, osteoblast differentiation, and bone formation. Furthermore, WNT/β-catenin signaling is over-activated in osteosarcoma and promotes tumor progression. Importantly, the WNT/β-catenin pathway normally activates RUNX2 gene expression during osteogenic lineage commitment. Therefore, we examined whether the WNT/β-catenin pathway controls the tumor-related elevation of RUNX2 expression in osteosarcoma. We analyzed protein levels and nuclear localization of β-catenin and RUNX2 in a panel of human osteosarcoma cell lines (SAOS, MG63, U2OS, HOS, G292, and 143B). In all six cell lines, β-catenin and RUNX2 are expressed to different degrees and localized in the nucleus and/or cytoplasm. SAOS cells have the highest levels of RUNX2 protein that is localized in the nucleus, while MG63 cells have the lowest RUNX2 levels which is mostly localized in the cytoplasm. Levels of β-catenin and RUNX2 protein are enhanced in HOS, G292, and 143B cells after treatment with the GSK3β inhibitor SB216763. Furthermore, small interfering RNA (siRNA)-mediated depletion of β-catenin inhibits RUNX2 expression in G292 cells. Thus, WNT/β-catenin activation is required for RUNX2 expression in at least some osteosarcoma cell types, where RUNX2 is known to promote expression of metastasis related genes. J. Cell. Biochem. 118: 3662-3674, 2017. © 2017 Wiley Periodicals, Inc.

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Section: Methodsmentioning

confidence: 99%

Wnt/β‐Catenin Signaling Activates Expression of the Bone‐Related Transcription Factor RUNX2 in Select Human Osteosarcoma Cell Types

Vega

Lucero

Araya

et al. 2017

J of Cellular Biochemistry

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“…Runx2 also known as core binding factor α1 (Cbfa1) is an important transcription factor involved in osteogenic differentiation of BMSCs. Its activation has been recognized as an initiation signal for the commitment of BMSCs to osteogenesis [47]. Actually, it induces osteogenesis both in vivo and in vitro by binding with the cis-element of the osteocalcin gene and initiates the transcription of some osteogenic genes [48].…”

Section: Transcription Factors Involved In Osteogenic Differentiationmentioning

confidence: 99%

Senile Osteoporosis: The Involvement of Differentiation and Senescence of Bone Marrow Stromal Cells

Qadir

Liang

et al. 2020

IJMS

156

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Senile osteoporosis has become a worldwide bone disease with the aging of the world population. It increases the risk of bone fracture and seriously affects human health. Unlike postmenopausal osteoporosis which is linked to menopause in women, senile osteoporosis is due to aging, hence, affecting both men and women. It is commonly found in people with more than their 70s. Evidence has shown that with age increase, bone marrow stromal cells (BMSCs) differentiate into more adipocytes rather than osteoblasts and undergo senescence, which leads to decreased bone formation and contributes to senile osteoporosis. Therefore, it is necessary to uncover the molecular mechanisms underlying the functional changes of BMSCs. It will benefit not only for understanding the senile osteoporosis development, but also for finding new therapies to treat senile osteoporosis. Here, we review the recent advances of the functional alterations of BMSCs and the related mechanisms during senile osteoporosis development. Moreover, the treatment of senile osteoporosis by aiming at BMSCs is introduced.

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“…These findings indicated that Runx2 plays an essential role in osteogenic differentiation and demonstrated the ability to use Runx2 gene transfer to enhance the differentiation of MSCs into osteocytes (Zhao et al, 2005). The post-mitotic symmetric segregation of Runx2 mRNA to progeny cells has been also found to support the maintenance of osteogenic lineage commitment and osteoblast phenotype (Varela et al, 2015). Homeobox protein Hox-B7 (HOXB7) over-expression affected the mRNA expression of the key transcription factor, Runx2, and promotes osteogenic differentiation.…”

Section: Introductionmentioning

confidence: 99%

Key transcription factors in the differentiation of mesenchymal stem cells

2016

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Mesenchymal stem cells (MSCs) are multipotent cells that represent a promising source for regenerative medicine. MSCs are capable of osteogenic, chondrogenic, adipogenic and myogenic differentiation. Efficacy of differentiated MSCs to regenerate cells in the injured tissues requires the ability to maintain the differentiation toward the desired cell fate. Since MSCs represent an attractive source for autologous transplantation, cellular and molecular signaling pathways and micro-environmental changes have been studied in order to understand the role of cytokines, chemokines, and transcription factors on the differentiation of MSCs. The differentiation of MSC into a mesenchymal lineage is genetically manipulated and promoted by specific transcription factors associated with a particular cell lineage. Recent studies have explored the integration of transcription factors, including Runx2, Sox9, PPARγ, MyoD, GATA4, and GATA6 in the differentiation of MSCs. Therefore, the overexpression of a single transcription factor in MSCs may promote trans-differentiation into specific cell lineage, which can be used for treatment of some diseases. In this review, we critically discussed and evaluated the role of transcription factors and related signaling pathways that affect the differentiation of MSCs toward adipocytes, chondrocytes, osteocytes, skeletal muscle cells, cardiomyocytes, and smooth muscle cells.

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Mitotic Inheritance of mRNA Facilitates Translational Activation of the Osteogenic-Lineage Commitment Factor Runx2 in Progeny of Osteoblastic Cells

Cited by 19 publications

References 87 publications

Wnt/β‐Catenin Signaling Activates Expression of the Bone‐Related Transcription Factor RUNX2 in Select Human Osteosarcoma Cell Types

Wnt/β‐Catenin Signaling Activates Expression of the Bone‐Related Transcription Factor RUNX2 in Select Human Osteosarcoma Cell Types

Senile Osteoporosis: The Involvement of Differentiation and Senescence of Bone Marrow Stromal Cells

Key transcription factors in the differentiation of mesenchymal stem cells

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