Li-ya Su1, Ying-xu Shi1, Mei-rong Yan1, Yaguang Xi2, Xiu-lan Su1. 1. Clinical Medicine Research Center of the Affiliated Hospital, Inner Mongolia Medical University, Hohhot 010050, China. 2. University of South Alabama Mitchell Cancer Institute, Mobile, AL 36604, USA.
Abstract
AIM: We have reported novel anticancer bioactive peptides (ACBPs) that show tumor-suppressive activities in human gastric cancer, leukemia, nasopharyngeal cancer, and gallbladder cancer. In this study, we investigated the effects of ACBPs on human colorectal cancer and the underlying mechanisms. METHODS: Cell growth and apoptosis of human colorectal tumor cell line HCT116 were measured using cell proliferation assay and flow cytometry, respectively. The expression levels of PARP, p53 and Mcl1A were assessed with Western blotting and immunohistochemistry. For evaluation of the in vivo antitumor activity of ACBPs, HCT116 xenograft nude mice were treated with ACBPs (35 μg/mL, ip) for 10 days. RESULTS: Treatment of HCT116 cells with ACBPs (35 μg/mL) for 4-6 days significantly inhibited the cell growth. Furthermore, treatment of HCT116 cells with ACBPs (35 μg/mL) for 6-12 h significantly enhanced UV-induced apoptosis, increased the expression of PARP and p53, and decreased the expression of Mcl-1. Administration of ACBPs did not change the body weight of HCT116 xenograft nude mice, but decreased the tumor growth by approximately 43%, and increased the expression of PARP and p53, and decreased the expression of Mcl-1 in xenograft mouse tumor tissues. CONCLUSION: Administration of ACBPs inhibits human colorectal tumor cell growth and induces apoptosis in vitro and in vivo through modulating the PARP-p53-Mcl-1 signaling pathway.
AIM: We have reported novel anticancer bioactive peptides (ACBPs) that show tumor-suppressive activities in humangastric cancer, leukemia, nasopharyngeal cancer, and gallbladder cancer. In this study, we investigated the effects of ACBPs on humancolorectal cancer and the underlying mechanisms. METHODS: Cell growth and apoptosis of humancolorectal tumor cell line HCT116 were measured using cell proliferation assay and flow cytometry, respectively. The expression levels of PARP, p53 and Mcl1A were assessed with Western blotting and immunohistochemistry. For evaluation of the in vivo antitumor activity of ACBPs, HCT116 xenograft nude mice were treated with ACBPs (35 μg/mL, ip) for 10 days. RESULTS: Treatment of HCT116 cells with ACBPs (35 μg/mL) for 4-6 days significantly inhibited the cell growth. Furthermore, treatment of HCT116 cells with ACBPs (35 μg/mL) for 6-12 h significantly enhanced UV-induced apoptosis, increased the expression of PARP and p53, and decreased the expression of Mcl-1. Administration of ACBPs did not change the body weight of HCT116 xenograft nude mice, but decreased the tumor growth by approximately 43%, and increased the expression of PARP and p53, and decreased the expression of Mcl-1 in xenograft mousetumor tissues. CONCLUSION: Administration of ACBPs inhibits humancolorectal tumor cell growth and induces apoptosis in vitro and in vivo through modulating the PARP-p53-Mcl-1 signaling pathway.
Authors: Daniel P Stewart; Brian Koss; Madhavi Bathina; Rhonda M Perciavalle; Kristen Bisanz; Joseph T Opferman Journal: Mol Cell Biol Date: 2010-04-12 Impact factor: 4.272
Authors: Brian Koss; Jeffrey Morrison; Rhonda M Perciavalle; Harpreet Singh; Jerold E Rehg; Richard T Williams; Joseph T Opferman Journal: Blood Date: 2013-07-23 Impact factor: 22.113