ArticleCancer chemotherapy and pharmacology2021
Demethoxycucumin protects MDA-MB-231 cells induced bone destruction through JNK and ERK pathways inhibition.
Article in Cancer chemotherapy and pharmacology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 14 citations in OpenAlex.
- Article
- Binary curcuminoid complex CRE-Bin inhibits osteoclast differentiation by suppressing the canonical NF-κB signaling pathway and modulating microRNA-223 expression.Scientific reports · 2025Article
- Screening of Oxidative Stress-related Biomarkers and Antioxidant Drugs for Polycystic Ovary Syndrome Based on Bioinformatics and Molecular Docking.Reproductive sciences (Thousand Oaks, Calif.) · 2025Article
- Lung cancer exosomal Gal3BP promotes osteoclastogenesis with potential connotation in osteolytic metastasis.Scientific reports · 2024Article
- Peripheral Mechanism of Cancer-Induced Bone Pain.Neuroscience bulletin · 2024Review
- The role of Clec11a in bone construction and remodeling.Frontiers in endocrinology · 2024Review
- Curcuminoids as Cell Signaling Pathway Modulators: A Potential Strategy for Cancer Prevention.Current medicinal chemistry · 2024Review
- Modified Curcuminoid-Rich Extract Liposomal CRE-SDInhibits Osteoclastogenesis via the Canonical NF-κB Signaling Pathway.Pharmaceutics · 2023Article
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Authors and funding
12 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Bone is the most common late metastasis of breast cancer. Bone metastasis causes not only severe bone pain, but also bone-related diseases such as pathological fractures, which are closely related to osteoclasts. The effects of demethoxycurcumin (DMC) on osteoclast biology has not been investigated. In this study, we explored the effects of DMC on MDA-MB-231 cells, MCF-7 cells, and osteoclasts induced by RANKL in vitro, as well as the protective effect on bone destruction of tumor bone metastasis in vivo. DMC showed inhibitory effect on the migration and promotes the apoptosis of MDA-MB-231 and MCF-7 cells. At the same time, DMC inhibited osteoclast maturation and mature osteoclast bone resorption in a dose-dependent manner, and suppressed the expression of osteoclast marker genes TRAP, CTSK, MMP9, V-ATPase-d2 and DC-STAMP significantly. Biochemical data showed that DMC inhibited tumor cells and osteoclasts by inhibiting the early activation of ERK and JNK MAPK pathway. Consistent with the results in vitro, we confirmed that DMC protects bone destruction caused by tumor metastasis in vivo. In short, our study confirmed that DMC could be used as a potential drug for the treatment of tumor bone destruction.
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