title: Anticancer bioactive peptides suppress human colorectal tumor cell growth and induce apoptosis via modulating the PARP-p53-Mcl-1 signaling pathway.
abstract: OBJECTIVE
  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.
  
  
  CONCLUSIONS
  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.
authors.affiliation: Clinical Medicine Research Center of the Affiliated Hospital, Inner Mongolia Medical University, Hohhot 010050, China.
authors.forename: Li-ya
authors.initials: LY
authors.lastname: Su
authors.affiliation: Clinical Medicine Research Center of the Affiliated Hospital, Inner Mongolia Medical University, Hohhot 010050, China.
authors.forename: Ying-xu
authors.initials: YX
authors.lastname: Shi
authors.affiliation: Clinical Medicine Research Center of the Affiliated Hospital, Inner Mongolia Medical University, Hohhot 010050, China.
authors.forename: Mei-rong
authors.initials: MR
authors.lastname: Yan
authors.affiliation: University of South Alabama Mitchell Cancer Institute, Mobile, AL 36604, USA.
authors.forename: Yaguang
authors.initials: Y
authors.lastname: Xi
authors.affiliation: Clinical Medicine Research Center of the Affiliated Hospital, Inner Mongolia Medical University, Hohhot 010050, China.
authors.forename: Xiu-lan
authors.initials: XL
authors.lastname: Su
mesh_terms: D000818:Animals; D000970:Antineoplastic Agents / Q000627:therapeutic use*; D017209:Apoptosis / Q000187:drug effects; D049109:Cell Proliferation / Q000187:drug effects; D003106:Colon / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D015179:Colorectal Neoplasms / Q000188:drug therapy* / Q000378:metabolism / Q000473:pathology; D045325:HCT116 Cells; D006801:Humans; D008297:Male; D008819:Mice, Nude; D064549:Myeloid Cell Leukemia Sequence 1 Protein / Q000378:metabolism*; D010455:Peptides / Q000627:therapeutic use*; D011065:Poly(ADP-ribose) Polymerases / Q000378:metabolism*; D012007:Rectum / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D015398:Signal Transduction / Q000187:drug effects*; D016159:Tumor Suppressor Protein p53 / Q000378:metabolism*
chemical_list: D000970:Antineoplastic Agents; C579095:MCL1 protein, human; D064549:Myeloid Cell Leukemia Sequence 1 Protein; D010455:Peptides; D016159:Tumor Suppressor Protein p53; D011065:Poly(ADP-ribose) Polymerases