Bone Marrow-Derived Mesenchymal Stem Cells Migrate toward Hormone-Insensitive Prostate Tumor Cells Expressing TGF-β via N-Cadherin

Noh, Jinok; Yu, Jinyeong; Kim, Wootak; Park, Aran; Park, Ki‐Sook

doi:10.3390/biomedicines9111572

Cited by 4 publications

(1 citation statement)

References 53 publications

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“…In addition, TGF-β-induced DACT1 suppressed WNT signaling and promoted breast and prostate cancer bone metastasis [115]. In both prostate and breast cancer, TGF-β was found to stimulate tumor microenvironment by modulating the recruitment of bone marrow-derived mesenchymal stem cells (BMSCs) into the tumor, mediated by transmembrane protein neural cadherin (N-cadherin) [116,117]. More recently, prostate cancerderived GDF15 was found to increase the osteoclastogenic potential of osteoblasts, which secrete RANKL and CCL2 to promote bone resorption [118].…”

Section: Growth Factors Mediating Bone Defectsmentioning

confidence: 99%

Muscle and Bone Defects in Metastatic Disease

Pauk

Saito

Hesse

et al. 2022

Curr Osteoporos Rep

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Purpose of Review The present review addresses most recently identified mechanisms implicated in metastasis-induced bone resorption and muscle-wasting syndrome, known as cachexia. Recent Findings Metastatic disease in bone and soft tissues is often associated with skeletal muscle defects. Recent studies have identified a number of secreted molecules and extracellular vesicles that contribute to cancer cell growth and metastasis leading to bone destruction and muscle atrophy. In addition, alterations in muscle microenvironment including dysfunctions in hepatic and mitochondrial metabolism have been implicated in cancer-induced regeneration defect and muscle loss. Moreover, we review novel in vitro and animal models including promising new drug candidates for bone metastases and cancer cachexia. Summary Preservation of bone health could be highly beneficial for maintaining muscle mass and function. Therefore, a better understanding of molecular pathways implicated in bone and muscle crosstalk in metastatic disease may provide new insights and identify new strategies to improve current anticancer therapeutics.

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Section: Growth Factors Mediating Bone Defectsmentioning

confidence: 99%

Muscle and Bone Defects in Metastatic Disease

Pauk

Saito

Hesse

et al. 2022

Curr Osteoporos Rep

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Tissue Bioengineering and Regeneration in Implant Dentistry

2022

Essential Techniques of Alveolar Bone Augmentation in Implant Dentistry

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ZO-1 regulates the migration of mesenchymal stem cells in cooperation with α-catenin in response to breast tumor cells

Park,

Choi,

et al. 2024

Cell Death Discov.

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AbstractsMesenchymal stem cells are recruited from the bone marrow into breast tumors, contributing to the creation of a tumor microenvironment that fosters tropism for breast tumors. However, the intrinsic mechanisms underlying the recruitment of bone marrow-derived mesenchymal stem cells (MSCs) into the breast tumor microenvironment are still under investigation. Our discoveries identified zonula occludens-1 (ZO-1) as a specific intrinsic molecule that plays a vital role in mediating the collective migration of MSCs towards breast tumor cells and transforming growth factor beta (TGF-β), which is a crucial factor secreted by breast tumor cells. Upon migration in response to MDA-MB-231 cells and TGF-β, MSCs showed increased formation of adherens junction-like structures (AJs) expressing N-cadherin and α-catenin at their cell-cell contacts. ZO-1 was found to be recruited into the AJs at the cell-cell contacts between MSCs. Additionally, ZO-1 collaborated with α-catenin to regulate AJ formation, dependently on the SH3 and GUK domains of the ZO-1 protein. ZO-1 knockdown led to the impaired migration of MSCs in response to the stimuli and subsequent downregulation of AJs formation at the cell-cell contacts during MSCs migration. Overall, our study highlights the novel role of ZO-1 in guiding MSC migration towards breast tumor cells, suggesting its potential as a new strategy for controlling and re-engineering the breast tumor microenvironment.

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Bone Marrow-Derived Mesenchymal Stem Cells Migrate toward Hormone-Insensitive Prostate Tumor Cells Expressing TGF-β via N-Cadherin

Cited by 4 publications

References 53 publications

Muscle and Bone Defects in Metastatic Disease

Muscle and Bone Defects in Metastatic Disease

Tissue Bioengineering and Regeneration in Implant Dentistry

ZO-1 regulates the migration of mesenchymal stem cells in cooperation with α-catenin in response to breast tumor cells

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