Fructose 1,6-bisphosphate inhibits osteoclastogenesis by attenuating RANKL-induced NF-κB/NFATc-1

Wilches-Buitrago, L.; Viacava, Paula Ramos; Cunha, Fernando; Alves‐Filho, José C.; Fukada, Sandra Yasuyo

doi:10.1007/s00011-019-01228-w

Cited by 11 publications

(4 citation statements)

References 24 publications

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“…[ 27 ] Studies also reported that many substances can disturb osteoclast differentiation through regulating NFATc‐1. For example, fructose 1,6‐bisphosphate can inhibit osteoclastogenesis by attenuating RANKL‐induced NF‐κB/NFATc‐1, [ 36 ] and other compounds including a flavonoids, [ 37 ] and (‐)‐Epicatechin 3‐O‐β‐ d ‐allopyranoside (ECAP) [ 38 ] could also regulate the expression of NFATc‐1. In this study, we investigated that whether miR‐506 suppressed breast cancer‐induced bone metastasis by directly targeting NFATc1.…”

Section: Discussionmentioning

confidence: 99%

MicroRNA‐506 ameliorates breast cancer‐induced osteolytic bone metastasis via the NFATc‐1 signaling pathway

Qin

Kong

et al. 2022

J Biochem & Molecular Tox

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Breast cancer is becoming a common life-threatening disease, especially in women, along with higher incidence and mortality. MicroRNA (miR)−506 was reported to participate in breast cancer progression, while the role of miR-506 in breast cancer-induced osteolytic bone metastasis is unclear. In the present study, we found significant downregulation of miR-506 in breast cancer tissues and cell lines. Overexpression of miR-506 notably reduced the proliferative, migratory and invasive rates of MCF7 and MDA-MB-231 cells, and reduced the production of inflammatory factors IL-6 and TNF-α in MCF7 cells. Moreover, overexpression of miR-506 obviously inhibited tumor growth in an in vivo animal model. In addition, overexpression of miR-560 efficiently attenuated breast cancer-induced osteolysis in vivo, which was characterized by increased bone volume/total volume (BT/TV), trabecular number (Tb. N), and trabecular thickness (Tb. Th), as well as the reduced trabecular separation (Tb. Sp). The nuclear factor of activated T cell cytoplasmic 1 (NFATc1) was identified as a downstream target of miR-506, and overexpression of miR-506 could inhibit breast cancer progression by targeting NFATc1. Furthermore, our results showed that NFATc-1 might participate in the inhibition of miR-506 on breast cancer-induced osteolysis. In conclusion, our findings provide insights into understanding the pathogenesis of breast cancer and breast cancer-induced osteolytic bone metastasis, and miR-506 might serve as a novel biomarker for this disease.

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Section: Discussionmentioning

confidence: 99%

MicroRNA‐506 ameliorates breast cancer‐induced osteolytic bone metastasis via the NFATc‐1 signaling pathway

Qin

Kong

et al. 2022

J Biochem & Molecular Tox

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“…In addition, glycolytic intermediates or products themselves have been shown to affect osteoclast differentiation and activity. As such, fructose 1,6-bisphosphate has been reported to suppress RANKL-induced osteoclastogenesis and TRAP activity through NF-kB/NFATc1 pathway inhibition in bone-marrow-derived murine osteoclasts when given in high concentrations (100 µM, 300 µM) in vitro [ 41 ]. Furthermore, lactate production progressively increases during osteoclast development, and correspondingly, the expression of LDH, which catalyzes the reaction of pyruvate into lactate, is elevated in mature mouse bone marrow-derived osteoclasts [ 42 ].…”

Section: Glycolysis As a Relay In Osteoclast Functionmentioning

confidence: 99%

Novel Insights into Osteoclast Energy Metabolism

Ledesma-Colunga,

Passin,

Lademann

et al. 2023

Curr Osteoporos Rep

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Purpose of Review Osteoclasts are crucial for the dynamic remodeling of bone as they resorb old and damaged bone, making space for new bone. Metabolic reprogramming in these cells not only supports phenotypic changes, but also provides the necessary energy for their highly energy-consuming activity, bone resorption. In this review, we highlight recent developments in our understanding of the metabolic adaptations that influence osteoclast behavior and the overall remodeling of bone tissue. Recent Findings Osteoclasts undergo metabolic reprogramming to meet the energy demands during their transition from precursor cells to fully mature bone-resorbing osteoclasts. Recent research has made considerable progress in pinpointing crucial metabolic adaptations and checkpoint proteins in this process. Notably, glucose metabolism, mitochondrial biogenesis, and oxidative respiration were identified as essential pathways involved in osteoclast differentiation, cytoskeletal organization, and resorptive activity. Furthermore, the interaction between these pathways and amino acid and lipid metabolism adds to the complexity of the process. These interconnected processes can function as diverse fuel sources or have independent regulatory effects, significantly influencing osteoclast function. Summary Energy metabolism in osteoclasts involves various substrates and pathways to meet the energetic requirements of osteoclasts throughout their maturation stages. This understanding of osteoclast biology may provide valuable insights for modulating osteoclast activity during the pathogenesis of bone-related disorders and may pave the way for the development of innovative therapeutic strategies.

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“…[27][28][29][30] Previous research has demonstrated the benefits of FBP for treating ischemia myocardia, promoting the survival of transplanted adipose tissue, maintaining bone homeostasis, and safeguarding hypoxia reperfusion ECs. [31][32][33][34][35][36] Therefore, it is a more efficient option to use high-energy intermediate FBP to directly supply energy to damaged tissue cells. However, FBP was originally administered intravenously in huge dosages without any targeting, which may lead to lactic acid poisoning, increased uric acid and other risks, and even life-threatening, and it is also challenging to maintain effective concentration when used locally.…”

Section: Introductionmentioning

confidence: 99%

Regulation of Glucose Metabolism for Cell Energy Supply In Situ via High‐Energy Intermediate Fructose Hydrogels

Lu,

Zhao,

Cai

et al. 2023

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The cellular functions, such as tissue‐rebuilding ability, can be directly affected by the metabolism of cells. Moreover, the glucose metabolism is one of the most important processes of the metabolism. However, glucose cannot be efficiently converted into energy in cells under ischemia hypoxia conditions. In this study, a high‐energy intermediate fructose hydrogel (HIFH) is developed by the dynamic coordination between sulfhydryl‐functionalized bovine serum albumin (BSA‐SH), the high‐energy intermediate in glucose metabolism (fructose‐1,6‐bisphosphate, FBP), and copper ion (Cu2+). This hydrogel system is injectable, self–healing, and biocompatible, which can intracellularly convert energy with high efficacy by regulating the glucose metabolism in situ. Additionally, the HIFH can greatly boost cell antioxidant capacity and increase adenosine triphosphate (ATP) in the ischemia anoxic milieu by roughly 1.3 times, improving cell survival, proliferation and physiological functions in vitro. Furthermore, the ischemic skin tissue model is established in rats. The HIFH can speed up the healing of damaged tissue by promoting angiogenesis, lowering reactive oxygen species (ROS), and eventually expanding the healing area of the damaged tissue by roughly 1.4 times in vivo. Therefore, the HIFH can provide an impressive perspective on efficient in situ cell energy supply of damaged tissue.

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Fructose 1,6-bisphosphate inhibits osteoclastogenesis by attenuating RANKL-induced NF-κB/NFATc-1

Cited by 11 publications

References 24 publications

MicroRNA‐506 ameliorates breast cancer‐induced osteolytic bone metastasis via the NFATc‐1 signaling pathway

MicroRNA‐506 ameliorates breast cancer‐induced osteolytic bone metastasis via the NFATc‐1 signaling pathway

Novel Insights into Osteoclast Energy Metabolism

Regulation of Glucose Metabolism for Cell Energy Supply In Situ via High‐Energy Intermediate Fructose Hydrogels

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