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Aloperine induces G2/M phase cell cycle arrest and apoptosis in HCT116 human colon cancer cells.

Abstract
Aloperine (ALO) is a quinolizidine alkaloid extracted from the leaves of Sophora alopecuroides (S. alopecuroides) and possesses anti-inflammatory, anti-allergenic, antitumor, and antiviral effects. In this study, when compared with seven other types of alkaloids extracted from S. alopecuroides, ALO treatment produced the most potent effects against HCT116 colon cancer cell types. ALO inhibited proliferation and induced apoptosis in HCT116 cells in a dose- and time-dependent manner as detected by MTT, clonogenic survival, and flow cytometric assays. Results of the western blot analysis and qPCR revealed that ALO increased the protein and mRNA of Bax and decreased Bcl-2 via the mitochondrial death pathway. In addition, ALO induced cell cycle arrest at the G2/M phase with a concomitant increase in p21 and p53 and a decrease in cyclin D1 and B1. ALO also inhibited phosphatidylinositol 3-kinase/Akt and JAK/Stat3. Generally, ALO exerted a significant anti-proliferative effect via apoptotic and cell cycle arrest induction in HCT116 cells. These results suggested that ALO should be investigated further as an agent of chemotherapeutic activity in human colon cancer.
AuthorsLi Zhang, Yanxin Zheng, Hongzhu Deng, Lei Liang, Juan Peng
JournalInternational journal of molecular medicine (Int J Mol Med) Vol. 33 Issue 6 Pg. 1613-20 (Jun 2014) ISSN: 1791-244X [Electronic] Greece
PMID24682388 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
Chemical References
  • Cyclin B1
  • Cyclin-Dependent Kinase Inhibitor p21
  • Piperidines
  • Quinolizidines
  • Tumor Suppressor Protein p53
  • Cyclin D1
  • aloperine
Topics
  • Apoptosis (drug effects, genetics)
  • Cell Cycle Checkpoints (drug effects, genetics)
  • Cell Division (drug effects, genetics)
  • Cyclin B1 (genetics, metabolism)
  • Cyclin D1 (genetics, metabolism)
  • Cyclin-Dependent Kinase Inhibitor p21 (genetics, metabolism)
  • G2 Phase (drug effects, genetics)
  • HCT116 Cells
  • Humans
  • Phosphatidylinositol 3-Kinases (genetics, metabolism)
  • Piperidines (pharmacology)
  • Quinolizidines
  • Tumor Suppressor Protein p53 (genetics, metabolism)

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