ReferenceID 2259
Magnoflorine inhibits the malignant phenotypes and increases cisplatin sensitivity of osteosarcoma cells via regulating miR-410-3p/HMGB1/NF-κB pathway
Life Sci
AIMS: Magnoflorine is an essential type of alkaloid and possesses anti-tumor activity in multiple cancers. Recent studies have demonstrated that magnoflorine plays tumor-suppressive roles in gastric and breast cancers. H
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- Reference Id
- 2259
- Evidence Id
- 18849
- Core Evidence Id
- 18849
- Source Reference Id
- 4555
- Herb2 Reference Id
- HBREF005352
- Subject Paper Key
- HBIN034216_32553931
- Pubmed Id
- 32553931
- Doi
- 10.1016/j.lfs.2020.117967
- Paper Title
- Magnoflorine inhibits the malignant phenotypes and increases cisplatin sensitivity of osteosarcoma cells via regulating miR-410-3p/HMGB1/NF-κB pathway
- Paper Abstract
- AIMS: Magnoflorine is an essential type of alkaloid and possesses anti-tumor activity in multiple cancers. Recent studies have demonstrated that magnoflorine plays tumor-suppressive roles in gastric and breast cancers. However, its role in osteosarcoma (OS) tumorigenesis is enigmatic. This study aimed to investigate the role and mechanism of magnoflorine in OS. MATERIALS AND METHODS: Two human OS cells (MG-63 and U-2 OS) were treated with different concentrations of magnoflorine. Cell viability and invasion were then detected by Cell Counting Kit-8 and Transwell assay, respectively. And the effects of magnoflorine on the epithelial-mesenchymal transition (EMT) and cisplatin sensitivity were also measured. To explore the potential mechanism, we assayed the influence of magnoflorine on the miR-410-3p/HMGB1/NF-kappaB signaling pathway. Additionally, rescue experiments were performed to further confirm the regulation mechanism of magnoflorine. KEY FINDINGS: Magnoflorine inhibited the viability, invasion, and EMT of OS cells in a dose-dependent manner. And it increased the sensitivity of OS cells to cisplatin. Magnoflorine significantly suppressed HMGB1 expression and NF-kappaB activation, but upregulated miR-410-3p level. Overexpression of HMGB1 promoted NF-kappaB activation and reversed the effects of magnoflorine on the viability, invasion, EMT and cisplatin sensitivity of OS cells. miR-410-3p mimic inhibited the EMT of OS cells, which was restored by HMGB1 upregulation. And miR-410-3p inhibitor abrogated the influence of magnoflorine on HMGB1 expression in OS cells. SIGNIFICANCE: Magnoflorine inhibited the malignant phenotypes and increased cisplatin sensitivity of OS cells via modulating miR-410-3p/HMGB1/NF-kappaB pathway. These results indicated that magnoflorine might be a novel drug for the treatment of OS.
- Journal
- Life Sci
- Publish Year
- 2020
- Experiment Subject
- human; human os cells; os cells
- Experiment Type
- Cell Experiment
- Phenotype Related
- Cancers; Gastric And Breast Cancers; Osteosarcoma
- Paper Title Cn
- Paper Title En
- Magnoflorine inhibits the malignant phenotypes and increases cisplatin sensitivity of osteosarcoma cells via regulating miR-410-3p/HMGB1/NF-κB pathway
- Bilingual Status
- semi_complete