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Celastrol inhibits colorectal cancer through TGF-β1/Smad signaling

Authors Jiang Z, Cao Q, Dai G, Wang J, Liu C, Lv L, Pan J

Received 17 September 2018

Accepted for publication 4 December 2018

Published 9 January 2019 Volume 2019:12 Pages 509—518

DOI https://doi.org/10.2147/OTT.S187817

Checked for plagiarism Yes

Review by Single-blind

Peer reviewers approved by Dr Amy Norman

Peer reviewer comments 3

Editor who approved publication: Dr William Cho


Zhitao Jiang,1,* Qianyu Cao,2,* Guoliang Dai,3 Jianchun Wang,1 Chundi Liu,1 Lingyan Lv,1 Jinhuo Pan4

1Department of Pharmacy Office, Zhangjiagang Hospital of Traditional Chinese Medicine Affiliated to Nanjing University of Chinese Medicine, Zhangjiagang, China; 2The First Clinical College, Nanjing University of Chinese Medicine, Nanjing, China; 3Department of Clinical Pharmacology, Affiliated Hospital of Nanjing University of Chinese Medicine, Nanjing, China; 4College of Pharmacy, Nanjing University of Chinese Medicine, Nanjing, China

*These authors contributed equally to this work

Background: There are few clinical challenges associated with the treatment of colorectal cancer (CRC). Studies have shown that TGF-β plays a crucial role in CRC. Importantly, celastrol, a major components of the root extract of the traditional Chinese herb Tripterygium wilfordii Hook F, has been shown to inhibit the growth, adhesion, and metastasis of human CRC cells through the inhibition of TGF-β1/Smad signaling.
Materials and methods: Real-time PCR and Western blot tests were proceeded to present TGF-β1, TGF-β receptor type I (TGFβRI), TGF-β receptor type II (TGFβRII), Smad2/3, p-Smad2/3, Smad4, and glyceraldehyde-3-phosphate dehydrogenase expression in human colon cancer cell samples.
Results: Our results indicated that celastrol can reduce the expression levels of TGF-β1, TGFβRI, and TGFβRII in HCT116 and SW620 cells. Furthermore, celastrol could also prevent the increase in Smad4 and p-Smad2/3 in HCT116 and SW620 cells.
Conclusion: Celastrol could inhibit tumor growth through TGF-β1/Smad signaling and might be a promising therapeutic component against CRC.

Keywords: celastrol, colorectal cancer, TGF-β1, Smad
 

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