Calycosin and genistein induce apoptosis by inactivation of HOTAIR/p-Akt signaling pathway in human breast cancer MCF-7 cells.

Abstract

BACKGROUND:

Calycosin and genistein are the two main components of isoflavones. Previously, we reported that these compounds display antitumor activities in the breast cancer cell lines MCF-7 and T47D. In the present study, we investigated the mechanism of action of calycosin and genistein, and their respective efficacies as potential therapies for the treatment of breast carcinoma in the clinic.

METHODS:

MCF-7 cells were treated with calycosin or genistein. Cell proliferation and apoptosis were measured using CCK8 assay and Hoechst 33258. The expression level of phosphorylated Akt protein was determined by western blotting. Expression level of HOTAIR was quantified by real-time PCR.

RESULTS:

Both calycosin and genistein inhibited proliferation and induced apoptosis in MCF-7 breast cancer cells, especially after treatment with calycosin. Treatment of MCF-7 cells with calycosin or genistein resulted in decreased phosphorylation of Akt, and decreased expression of its downstream target, HOTAIR.

CONCLUSION:

Calycosin is more effective in inhibiting breast cancer growth in comparison with genistein, through its regulation of Akt signaling pathways and HOTAIR expression.

• Authors: Jian Chen, Changrong Lin, Wang Yong, Yu Ye, Zhaoquan Huang
• Journal: Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology (Cell Physiol Biochem) Vol. 35 Issue 2 Pg. 722-8 ( 2015) ISSN: 1421-9778 [Electronic] Germany
• PMID: 25613518 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
• Copyright: © 2015 S. Karger AG, Basel.

Chemical References

• HOTAIR long untranslated RNA, human
• Isoflavones
• Phytoestrogens
• RNA, Long Noncoding
• 7,3'-dihydroxy-4'-methoxyisoflavone
• Genistein
• Proto-Oncogene Proteins c-akt

Topics

• Apoptosis
• Breast Neoplasms (metabolism, pathology)
• Cell Line, Tumor
• Cell Proliferation (drug effects)
• Down-Regulation
• Female
• Genistein (pharmacology)
• Humans
• Isoflavones (pharmacology)
• MCF-7 Cells
• Phosphorylation
• Phytoestrogens (pharmacology)
• Proto-Oncogene Proteins c-akt (genetics, metabolism)
• RNA, Long Noncoding (genetics, metabolism)
• Signal Transduction (drug effects)