2'-Hydroxychalcone Induces Autophagy and Apoptosis in Breast Cancer Cells via the Inhibition of the NF-κB Signaling Pathway: In Vitro and In Vivo Studies.
Xiao WangYongjie LiangBohan ZhangLixin HeWenxuan LiWenwen ZhangChengzong LiLihong LuoTalha UmarHuili FengChangwei QiuPublished in: Nutrients (2024)
2'-Hydroxychalcone is a hydroxyl derivative of chalcones, which are biosynthetic precursors of flavonoids and rich in the human diet. The anticancer activity of 2'-hydroxychalcone has been reported in several cancers but remains to be investigated in breast cancer. In the current study, 2'-hydroxychalcone showed significant cytotoxicity against breast cancer cell lines MCF-7 and CMT-1211. It could inhibit breast cancer cell proliferation, migration, and invasion in vitro and suppress tumor growth and metastasis in vivo. Mechanistic investigation revealed that the NF-κB pathway was significantly inhibited by 2'-hydroxychalcone treatment accompanied by an excessive intracellular accumulation of reactive oxygen species, induction of endoplasmic reticulum stress, and activation of JNK/MAPK. In addition, 2'-hydroxychalcone elevated the autophagic levels in breast cancer cells equipped with increasing numbers of autophagy vesicles and complete autophagic flux. Finally, autophagy-dependent apoptosis was observed in 2'-hydroxychalcone-induced cell death. In conclusion, 2'-hydroxychalcone enhances the autophagic levels and induces apoptosis in breast cancer cells, which could be contributed to the inhibition of the pro-survival NF-κB signaling, indicating a promising potential for 2'-hydroxychalcone in future anticancer drug development.
Keyphrases
- cell death
- signaling pathway
- endoplasmic reticulum stress
- breast cancer cells
- pi k akt
- induced apoptosis
- cell cycle arrest
- oxidative stress
- cell proliferation
- reactive oxygen species
- epithelial mesenchymal transition
- lps induced
- endothelial cells
- cell cycle
- nuclear factor
- diabetic rats
- high glucose
- physical activity
- childhood cancer
- anti inflammatory
- risk assessment
- young adults
- mass spectrometry
- inflammatory response
- free survival