7, 8-Dihydroxyflavone suppresses proliferation and induces apoptosis of human osteosarcoma cells. (21st May 2021)
- Record Type:
- Journal Article
- Title:
- 7, 8-Dihydroxyflavone suppresses proliferation and induces apoptosis of human osteosarcoma cells. (21st May 2021)
- Main Title:
- 7, 8-Dihydroxyflavone suppresses proliferation and induces apoptosis of human osteosarcoma cells
- Authors:
- Zhao, Jing
Li, Peifeng
Zhu, Hua
Ge, Fengqin
Liu, Jie
Xia, Jingjun
Hang, Pengzhou - Abstract:
- Abstract: Recent studies suggest that 7, 8-dihydroxyflavone (7, 8-DHF) inhibits the development of several tumors. However, its role in osteosarcoma (OS) remains unknown. This study was designed to investigate the effects and underlying mechanisms of 7, 8-DHF that may influence OS development. Human OS cell lines (U2OS and 143B) were treated with 7, 8-DHF; cell viability and cell migration were assessed by methylthiazolyldiphenyl-tetrazolium bromide (MTT) assay and wound-healing assay, respectively; and cell death and apoptosis were evaluated by LIVE/DEAD staining and terminal deoxynucleotidyl transferase (TdT) dUTP nick-end labeling (TUNEL) assay, respectively. Reactive oxygen species production was measured using 2, 7-dichlorodihydrofluorescein diacetate probe. Akt, Bcl-xL/Bcl-2 asociated death promoter (Bad), p38 mitogen-activated protein kinase (MAPK), extracellular regulated protein kinase (ERK), and c-Jun N-terminal kinase (JNK) expression and their respective phosphorylation levels were detected by western blot analysis. We found that 7, 8-DHF reduced cell viability in a dose-dependent manner and also promoted apoptosis, inhibited migration, and induced oxidative stress in OS cells. Moreover, 7, 8-DHF inhibited Akt, Bad, and p38MAPK, but activated ERK and JNK signals. In summary, our results suggest that 7, 8-DHF inhibits OS progression, possibly by regulating Akt/Bad and MAPK signaling. These findings provide new evidence for the pharmacological effects of 7, 8-DHFAbstract: Recent studies suggest that 7, 8-dihydroxyflavone (7, 8-DHF) inhibits the development of several tumors. However, its role in osteosarcoma (OS) remains unknown. This study was designed to investigate the effects and underlying mechanisms of 7, 8-DHF that may influence OS development. Human OS cell lines (U2OS and 143B) were treated with 7, 8-DHF; cell viability and cell migration were assessed by methylthiazolyldiphenyl-tetrazolium bromide (MTT) assay and wound-healing assay, respectively; and cell death and apoptosis were evaluated by LIVE/DEAD staining and terminal deoxynucleotidyl transferase (TdT) dUTP nick-end labeling (TUNEL) assay, respectively. Reactive oxygen species production was measured using 2, 7-dichlorodihydrofluorescein diacetate probe. Akt, Bcl-xL/Bcl-2 asociated death promoter (Bad), p38 mitogen-activated protein kinase (MAPK), extracellular regulated protein kinase (ERK), and c-Jun N-terminal kinase (JNK) expression and their respective phosphorylation levels were detected by western blot analysis. We found that 7, 8-DHF reduced cell viability in a dose-dependent manner and also promoted apoptosis, inhibited migration, and induced oxidative stress in OS cells. Moreover, 7, 8-DHF inhibited Akt, Bad, and p38MAPK, but activated ERK and JNK signals. In summary, our results suggest that 7, 8-DHF inhibits OS progression, possibly by regulating Akt/Bad and MAPK signaling. These findings provide new evidence for the pharmacological effects of 7, 8-DHF that may improve drug therapy for OS patients. … (more)
- Is Part Of:
- Acta biochimica et biophysica Sinica. Volume 53:Number 7(2021)
- Journal:
- Acta biochimica et biophysica Sinica
- Issue:
- Volume 53:Number 7(2021)
- Issue Display:
- Volume 53, Issue 7 (2021)
- Year:
- 2021
- Volume:
- 53
- Issue:
- 7
- Issue Sort Value:
- 2021-0053-0007-0000
- Page Start:
- 903
- Page End:
- 911
- Publication Date:
- 2021-05-21
- Subjects:
- osteosarcoma -- 7, 8-dihydroxyflavone -- proliferation -- apoptosis -- ROS
Biochemistry -- Periodicals
Biophysics -- Periodicals
572.05 - Journal URLs:
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http://www.blackwellpublishing.com/journal.asp?ref=1672-9145&site=1 ↗ - DOI:
- 10.1093/abbs/gmab060 ↗
- Languages:
- English
- ISSNs:
- 1672-9145
- Deposit Type:
- Legaldeposit
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