Open Access


Read more
image01

Online Manuscript Submission


Read more
image01

Submitted Manuscript Trail


Read more
image01

Online Payment


Read more
image01

Online Subscription


Read more
image01

Email Alert



Read more
image01

Original Research Article | OPEN ACCESS

Glutinol inhibits the proliferation of human ovarian cancer cells via PI3K/AKT signaling pathway

Yuanyuan Chen1, Juan Li2

1Department of Radiation Oncology, Women’s Hospital; 2Department of Radiation Oncology, Affiliated Hangzhou Cancer Hospital, School of Medicine, Zhejiang University, HangZhou, ZheJiang 310002, China.

For correspondence:-  Juan Li   Email: jlu.edu.1@gmail.com   Tel:+8657156006302

Accepted: 24 June 2021        Published: 29 July 2021

Citation: Chen Y, Li J. Glutinol inhibits the proliferation of human ovarian cancer cells via PI3K/AKT signaling pathway. Trop J Pharm Res 2021; 20(7):1331-1335 doi: 10.4314/tjpr.v20i7.2

© 2021 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..

Abstract

Purpose: To investigate the anticancer effect of glutinol on OVACAR3 human ovarian cancer cells, and to elucidate the underlying molecular mechanisms.
Methods: Cell viability was determined using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT) assay. Cell cycle distribution, reactive oxygen species (ROS) and mitochondrial membrane potential were measured via flow cytometry, while protein expression levels were determined with western blotting assay.
Results: Glutinol exerted significant growth-inhibitory effects on human OVACAR3 cells, but interestingly, it exhibited comparatively lower cytotoxic effects against normal SV40 cells. The IC50 of glutinol against human OVACAR3 cells was 6 µM, while the IC50 against normal SV40 cells was 60 µM. Flow cytometric analysis showed an increase in population of OVACAR3 cells in G2/M phase from 4.02 % in control to 29.05 % on treatment with 12 µM glutinol, suggestive of G2/M phase arrest. The G2/M arrest of OVACAR3 cells was also accompanied by suppression of cyclin B1. It was also found that increases in ROS levels and decreases in MMP activities contributed to the glutinol-induced antiproliferative effects on human OVACAR3 cells. Moreover, glutinol deactivated the PI3K/AKT signaling pathway in OVACAR-3 ovarian cancer cells.
Conclusion: Glutinol exerted potent anticancer effects against human ovarian cancer. Thus, it might be of potential benefit in the treatment of ovarian cancer.

Keywords: Ovarian cancer, Glutinol, Cell cycle arrest, Chemotherapy, Triterpenes

Impact Factor
Thompson Reuters (ISI): 0.6 (2023)
H-5 index (Google Scholar): 49 (2023)

Article Tools

Share this article with



Article status: Free
Fulltext in PDF
Similar articles in Google
Similar article in this Journal:

Archives

2024; 23: 
1,   2,   3,   4,   5,   6,   7,   8,   9,   10
2023; 22: 
1,   2,   3,   4,   5,   6,   7,   8,   9,   10,   11,   12
2022; 21: 
1,   2,   3,   4,   5,   6,   7,   8,   9,   10,   11,   12
2021; 20: 
1,   2,   3,   4,   5,   6,   7,   8,   9,   10,   11,   12
2020; 19: 
1,   2,   3,   4,   5,   6,   7,   8,   9,   10,   11,   12
2019; 18: 
1,   2,   3,   4,   5,   6,   7,   8,   9,   10,   11,   12
2018; 17: 
1,   2,   3,   4,   5,   6,   7,   8,   9,   10,   11,   12
2017; 16: 
1,   2,   3,   4,   5,   6,   7,   8,   9,   10,   11,   12
2016; 15: 
1,   2,   3,   4,   5,   6,   7,   8,   9,   10,   11,   12
2015; 14: 
1,   2,   3,   4,   5,   6,   7,   8,   9,   10,   11,   12
2014; 13: 
1,   2,   3,   4,   5,   6,   7,   8,   9,   10,   11,   12
2013; 12: 
1,   2,   3,   4,   5,   6
2012; 11: 
1,   2,   3,   4,   5,   6
2011; 10: 
1,   2,   3,   4,   5,   6
2010; 9: 
1,   2,   3,   4,   5,   6
2009; 8: 
1,   2,   3,   4,   5,   6
2008; 7: 
1,   2,   3,   4
2007; 6: 
1,   2,   3,   4
2006; 5: 
1,   2
2005; 4: 
1,   2
2004; 3: 
1
2003; 2: 
1,   2
2002; 1: 
1,   2

News Updates