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Trans-chalcone suppresses tumor growth mediated at least in part by the induction of heme oxygenase-1 in breast cancer
- Source :
- Toxicological Research
- Publication Year :
- 2021
- Publisher :
- Springer Singapore, 2021.
-
Abstract
- Despite intensive research efforts in recent decades, cancer remains a leading cause of death worldwide. The chalcone family is a promising group of phytochemicals for therapeutic use against cancer development. Naturally-occurring chalcones, as well as synthetic chalcone analogues, have shown many beneficial biological properties, including anti-inflammatory, antioxidant, and anti-cancer activities. In this report, trans-chalcone (TChal) was found to increase cell death in breast cancer cells, assessed using high content screening. Subsequently, using antibody array analysis, TChal was found to increase heme oxygenase-1 (HO-1) expression in TChal-treated breast cancer cells. Blocking of HO-1 by siRNA in breast cancer cells diminished the effect of TChal on cell growth inhibition. TChal-fed mice also showed less tumor growth compared to vehicle-fed mice. Overall, we found that TChal increases HO-1 expression in breast cancer cells, thereby enhancing anti-tumorigenesis. Our results suggest that HO-1 expression could be a potential new target of TChal for anti-tumorigenesis in breast cancer.
- Subjects :
- Chalcone
Programmed cell death
Health, Toxicology and Mutagenesis
Toxicology
03 medical and health sciences
chemistry.chemical_compound
0302 clinical medicine
Breast cancer
Antibody array
medicine
Heme
030304 developmental biology
0303 health sciences
Cell growth
business.industry
Xenograft
Cancer
medicine.disease
Trans-chalcone
Heme oxygenase
chemistry
Heme oxygenase-1
030220 oncology & carcinogenesis
High-content screening
Cancer research
High content screening
Original Article
business
Subjects
Details
- Language :
- English
- ISSN :
- 22342753 and 19768257
- Volume :
- 37
- Issue :
- 4
- Database :
- OpenAIRE
- Journal :
- Toxicological Research
- Accession number :
- edsair.doi.dedup.....b8e7107db138a7c87dcb472fe40c8bec