Colorectal cancer (CRC) is one of the most frequent malignant tumors. Signaling by the PI3K/AKT pathway is crucial for CRC development and progression, including proliferation and migration. Celastrol has an anticancer effect, but its mechanism needs to be determined. Here, we showed that celastrol suppressed CRC cell proliferation and migration. Celastrol treatment also decreased the PI3K/AKT pathway components, and MMP3 and MMP7 expression levels. In addition, knockdown of AKT, not mTOR, inhibited MMP3 and MMP7 expression levels and AKT silencing promoted the celastrol-induced effects on CRC cell proliferation and migration. Taken together, these findings indicated that the celastrol-induced antitumor effects were mediated through MMP3 and MMP7 by the PI3K/AKT signaling pathway. This is an open-access article distributed under the terms of the Creative Commons Attribution-Non Commercial-No Derivatives License 4.0 (CCBY-NC-ND), where it is permissible to download and share the work provided it is properly cited. The work cannot be changed in any way or used commercially without permission from the journal. http://ift.tt/1hexVwJ Correspondence to Wang Ling, PhD, PhD Program for Immunology, Department of Oncology, the First Affiliated Hospital of Dalian Medical University, No. 193, Lian-He Road, Dalian 116011, People's Republic of China Tel: +86 180 9887 6728; fax: +86 411 8363 5963; e-mail: 516245530@qq.com Received October 2, 2017 Accepted February 26, 2018 Copyright © 2018 Wolters Kluwer Health, Inc. All rights reserved.
from #ORL-AlexandrosSfakianakis via ola Kala on Inoreader http://ift.tt/2HIsN6q
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