CTSG Suppresses Colorectal Cancer Progression through Negative Regulation of Akt/mTOR/Bcl2 Signaling Pathway
》》Journal：International Journal of Biological Sciences
》》相关产品：MK-2206 dihydrochloride (SJ-MX0056) 和 SC79 (SJ-MX0341)
》》Abstract
Colorectal cancer (CRC) is the most common gastrointestinal tumor worldwide, which is a severe malignant disease that threatens mankind. Cathepsin G (CTSG) has been reported to be associated with tumorigenesis, whereas its role in CRC is still unclear. This investigation aims to determine the function of CTSG in CRC. Our results indicated that CTSG was inhibited in CRC tissues, and patients with CTSG low expression have poor overall survival. Functional experiments revealed that CTSG overexpression suppressed CRC cell progression in vitro and in vivo, whereas CTSG suppression supports CRC development cells in vitro and in vivo. Mechanistically, CTSG overexpression suppressed Akt/mTOR signaling mechanism and elevated apoptotic-associated markers, and CTSG silencing activated Akt/mTOR signaling mechanisms and inhibited apoptotic-associated markers. Furthermore, the Akt suppression signaling pathway by MK2206 abolishes CTSG-silenced expression-induced cell viability and Bcl2 up-regulation in vitro and in vivo. Altogether, these outcomes demonstrate that CTSG may act as a tumor suppressor gene via Akt/mTOR/Bcl2-mediated anti-apoptotic signaling inactivation, and CTSG represents a potential therapeutic target in CRC.
》》部分文献数据展示：
Fig 1：The control cells and stable knockdown expression RKO cells were treated with DMSO or MK2206 (5 μM) for 24 h and then subjected to Western-blot analysis with the showed antibodies.
Fig 2: CTSG reverses SC79-induced CRC cell proliferation. A. MTT demonstrated that CTSG reversed the enhanced proliferative ability of HT29 cells after SC79 pretreatment for 2 hours (5 μM). B. CTSG reduced the increased AKT phosphorylation caused by SC79. ***P < 0.001.
