Yu Chen1,
Zhenwu Wang2,
Mei Liu1,
Xiaodong Wang1 
,
Linghan Zhang3,
Can Gong1
For correspondence:- Xiaodong Wang Email: WGargilak@yahoo.com
Accepted: 22 August 2018 Published: 30 September 2018
Citation: Chen Y, Wang Z, Liu M, Wang X, Zhang L, Gong C. Globularifolin inhibits CAMA-1 human breast cancer cell line via cell cycle arrest, apoptosis and inhibition of PI3K/AKT signalling pathway. Trop J Pharm Res 2018; 17(9):1711-1716 doi: 10.4314/tjpr.v17i9.4
© 2018 The authors.
This is an Open Access article that uses a funding model which does not charge readers or their institutions for access and distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0) and the Budapest Open Access Initiative (http://www.budapestopenaccessinitiative.org/read), which permit unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited..
Purpose: To investigate the anticancer activity of globularifolin against CAMA-1 breast cancer cells.
Methods: The viability of CAMA-1 cells was assessed by MTT assay. DAPI and annexin V/PI staining were used for the determination of apoptotic cell death. Flow cytometry was employed for cell cycle analysis, while wound healing and immunoblotting assays were used to measure cell migration and protein ex
Results: Globularifolin decreased the viability of CAMA-1 breast cancer cells dose-dependently, with half-maximal inhibitory concentration (IC50) of 10 µM, relative to its IC50 of 65 µM against non-cancerous CMMT breast cells. It also initiated apoptotic cell death and cell cycle arrest. Moreover, it inhibited the migration of CAMA-1 breast cancer cells, and PI3K/AKT signalling cascade.
Conclusion: These results suggest that globularifolin has promising potential for use in the treatment of breast cancer
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