Chaetocin inhibits RANKL-induced osteoclast differentiation through reduction of Blimp1 in Raw264.7 cells

Zhao, Ning; Tsuda, Hiromasa; Murofushi, Takahisa; Imai, Kenichi; Ochiai, Kuniyasu; Yang, Pishan; Suzuki, Naoto

doi:10.1016/j.lfs.2015.10.027

Cited by 16 publications

(7 citation statements)

References 37 publications

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“…For differentiation of osteoclasts, RAW264.7 cells were cultured with 10% FBS DMEM containing 50 ng/mL of recombinant mouse RANKL (Sigma-Aldrich), 40 ng/mL recombinant mouse M-CSF (R&D, Minneapolis, Minnesota, USA) in the absence or presence of CCP at indicated concentrations for 4 days 25 26…”

Section: Methodsmentioning

confidence: 99%

Cervus and cucumis peptides ameliorates bone erosion in experimental arthritis by inhibiting osteoclastogenesis

Lin

Liu

et al. 2019

Lupus Sci Med

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ObjectiveRheumatoid arthritis is an autoimmune disease characterised by inflammation and bone loss, leading to joint destruction and deformity. The cervus and cucumis polypeptide (CCP) injection, one of the traditional Chinese medicine injections combined extracts from deer horn and sweet melon seeds, is widely used to treat arthritis and bone fracture in China. The present study investigated the therapeutic efficacy and mechanism of CCP on pathological immune cells and bone homoeostasis in rodent experimental arthritis.MethodsThe effects of CCP (4 mg/kg and 2 mg/kg) on clinical arthritis symptoms, bone erosion, proinflammatory cytokines and pathological immune cells induced by complete Freund’s adjuvant was evaluated in male Sprague-Dawley rats. The impacts of CCP (2 mg/kg) on joint erythema and swelling, production of pathogenic antibodies and the proportion of inflammatory cells were assessed in collagen-induced arthritis (CIA) in DBA/1J mice. Regulation of osteoclastogenesis by CCP was observed in the murine macrophage-like RAW264.7 cells treated with receptor activator of nuclear factor-κB ligand (RANKL) and macrophage colony-stimulating factor (M-CSF).ResultsCCP administration significantly prevented disease progression in both adjuvant-induced arthritis (AIA) rats and CIA mice. The therapeutic benefits were accompanied by reduction of paw oedema, reversed bone destruction, decreased pathological changes and osteoclast numbers in joints in AIA rats, as well as attenuated clinical manifestation and autoantibodies production in CIA mice. Meanwhile, in vitro supplemented of CCP concentration dependently inhibited RANKL/M-CSF-induced osteoclast differentiation, without showing cytotoxicity in RAW264.7 cells. Further, the presence of CCP dampened the augmented downstream signalling transduction as well as activation of osteoclast-specific genes and transcription factors induced by RANKL/M-CSF in RAW264.7 cells.ConclusionOur study suggested that the therapeutic effects of CCP in experimental arthritis could be attributed to its intervention on RANKL-induced osteoclastogenesis signalling pathway in osteoclast precursor cells.

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Section: Methodsmentioning

confidence: 99%

Cervus and cucumis peptides ameliorates bone erosion in experimental arthritis by inhibiting osteoclastogenesis

Lin

Liu

et al. 2019

Lupus Sci Med

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“…Chaetocin has been demonstrated to suppress cancer cells through the induction of apoptosis. In multiple lung cancer cells, its treatment activates endoplasmic reticulum stress, which results in the upregulation of ER stress response proteins, transcription factor ATF3, and CHOP, which further contributes to apoptosis in a death receptor 5 (DR5)-dependent manner (Zhao et al, 2015a). Treatment of chaetocin reduces cell growth by downregulating Blimp1 and RANKL (receptor activator of NFκB ligand) expression, which reduces osteoclast differentiation.…”

Section: Regulation Of Colorectal Cancer By Epigenetic Mechanismmentioning

confidence: 99%

“…Osteoclast gets differentiated from hematopoetic macrophage-like cells through the RANKL–RANK signaling system. Osteoclast formation is associated with the bone-responsive diseases (Zhao et al, 2015a). In B16F10 mouse melanoma cells, chaetocin inhibits IBMX (3-isobutyl-1-methylxanthine)-induced melanogenesis through activation of ERK (Bae et al, 2016).…”

Section: Regulation Of Colorectal Cancer By Epigenetic Mechanismmentioning

confidence: 99%

Drugs Targeting Epigenetic Modifications and Plausible Therapeutic Strategies Against Colorectal Cancer

Patnaik

Anupriya

2019

Front. Pharmacol.

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Genetic variations along with epigenetic modifications of DNA are involved in colorectal cancer (CRC) development and progression. CRC is the fourth leading cause of cancer-related deaths worldwide. Initiation and progression of CRC is the cumulation of a variety of genetic and epigenetic changes in colonic epithelial cells. Colorectal carcinogenesis is associated with epigenetic aberrations including DNA methylation, histone modifications, chromatin remodeling, and non-coding RNAs. Recently, epigenetic modifications have been identified like association of hypermethylated gene Claudin11 (CLDN11) with metastasis and prognosis of poor survival of CRC. DNA methylation of genes CMTM3, SSTR2, MDF1, NDRG4 and TGFB2 are potential epigenetic biomarkers for the early detection of CRC. Tumor suppressor candidate 3 (TUSC3) mRNA expression is silenced by promoter methylation, which promotes epidermal growth factor receptor (EGFR) signaling and rescues the CRC cells from apoptosis and hence leading to poor survival rate. Previous scientific evidences strongly suggest epigenetic modifications that contribute to anticancer drug resistance. Recent research studies emphasize development of drugs targeting histone deacetylases (HDACs) and DNA methyltransferase inhibitors as an emerging anticancer strategy. This review covers potential epigenetic modification targeting chemotherapeutic drugs and probable implementation for the treatment of CRC, which offers a strong rationale to explore therapeutic strategies and provides a basis to develop potent antitumor drugs.

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“…21,22 Later, further studies proved RAW264.7 cells could respond to stimuli in vitro and subsequently generate multinucleated cells with the hallmark characteristics expected for fully differentiated osteoclasts (RAW-OCs). RAW264.7 cell linage is well-characterized with regard to macrophage-mediated immune, metabolic and phagocytic functions 21 and is increasingly used and accepted as a cellular model of osteoclastogenic study; [24][25][26] however, with the vastly usage of RAW-OCs for understanding the osteocalstogenesis in the past two decades, there raised considerable requirements for the extensively understanding the RAW-OCs and associated cellular biological mechanisms. RAW264.7 cell linage is well-characterized with regard to macrophage-mediated immune, metabolic and phagocytic functions 21 and is increasingly used and accepted as a cellular model of osteoclastogenic study; [24][25][26] however, with the vastly usage of RAW-OCs for understanding the osteocalstogenesis in the past two decades, there raised considerable requirements for the extensively understanding the RAW-OCs and associated cellular biological mechanisms.…”

Section: Introductionmentioning

confidence: 99%

“…23 Therefore, RAW-OCs can be used for studying osteoclastogenesis through different methods for various study purposes, including: biochemical, immunological, physiological, molecular and functional assays according to various study procedures. RAW264.7 cell linage is well-characterized with regard to macrophage-mediated immune, metabolic and phagocytic functions 21 and is increasingly used and accepted as a cellular model of osteoclastogenic study; [24][25][26] however, with the vastly usage of RAW-OCs for understanding the osteocalstogenesis in the past two decades, there raised considerable requirements for the extensively understanding the RAW-OCs and associated cellular biological mechanisms. 27,28 On the other hand, document studies reported that during the osteoclastic induction, various stimuli might lead different cellular fates during the RAW-OC induction.…”

Section: Introductionmentioning

confidence: 99%

Overview of RAW264.7 for osteoclastogensis study: Phenotype and stimuli

Kong

Smith

Hao

2019

J Cellular Molecular Medi

121

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Bone homeostasis is preserved by the balance of maintaining between the activity of osteogenesis and osteoclastogenesis. However, investigations for the osteoclastogenesis were hampered by considerable difficulties associated with isolating and culturing osteoclast in vivo. As the alternative, stimuli‐induced osteoclasts formation from RAW264.7 cells (RAW‐OCs) have gain its importance for extensively osteoclastogenic study of bone diseases, such as rheumatoid arthritis, osteoporosis, osteolysis and periodontitis. However, considering the RAW‐OCs have not yet been well‐characterized and RAW264.7 cells are polymorphic because of a diverse phenotype of the individual cells comprising this cell linage, and different fate associated with various stimuli contributions. Thus, in present study, we provide an overview for current knowledge of the phenotype of RAW264.7 cells, as well as the current understanding of the complicated interactions between various stimuli and RAW‐OCs in the light of the recent progress.

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Chaetocin inhibits RANKL-induced osteoclast differentiation through reduction of Blimp1 in Raw264.7 cells

Cited by 16 publications

References 37 publications

Cervus and cucumis peptides ameliorates bone erosion in experimental arthritis by inhibiting osteoclastogenesis

Cervus and cucumis peptides ameliorates bone erosion in experimental arthritis by inhibiting osteoclastogenesis

Drugs Targeting Epigenetic Modifications and Plausible Therapeutic Strategies Against Colorectal Cancer

Overview of RAW264.7 for osteoclastogensis study: Phenotype and stimuli

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