Jaceosidin induces p53-dependent G2/M phase arrest in U87 glioblastoma cells.

Abstract

Flavonoid compounds have been shown to trigger cell cycle arrest at G0/G1, S and G2/M checkpoints, allowing cells to repair DNA damage before entry into mitosis. Jaceosidin, a flavonoid compound, has been reported to induce apoptosis in various cancer cell lines. In our previous study, we established that jaceosidin induces apoptosis in U87 glioblastoma cells through G2/M phase arrest. However the molecular mechanisms oremained unclear. In the present study, mRNA and protein expression levels of major cell cycle regulatory genes were analyzed by semi-quantitative RT-PCR and Western blot studies respectively. The results demonstrated that jaceosidin-induced G2/M phase arrest in U87 cells is associated with DNA fragmentation, up-regulation of p53 and p21 and subsequent down-regulation of cyclin B1 and CDK1 expression at mRNA as well as at protein level. These findings provide insights into jaceosidin-induced G2/M phase arrest in U87 glioblastoma cells.

• Authors: Muhammad Khan, Azhar Rasul, Fei Yi, Lili Zhong, Tonghui Ma
• Journal: Asian Pacific journal of cancer prevention : APJCP (Asian Pac J Cancer Prev) Vol. 12 Issue 12 Pg. 3235-8 ( 2011) ISSN: 2476-762X [Electronic] Thailand
• PMID: 22471459 (Publication Type: Journal Article)

Chemical References

• CCNB1 protein, human
• CDKN1A protein, human
• Cyclin B1
• Cyclin-Dependent Kinase Inhibitor p21
• Flavonoids
• RNA, Messenger
• TP53 protein, human
• Tumor Suppressor Protein p53
• jaceosidin
• CDC2 Protein Kinase

Topics

• Apoptosis (drug effects)
• Blotting, Western
• Brain Neoplasms (genetics, metabolism, pathology)
• CDC2 Protein Kinase (genetics, metabolism)
• Cell Division (drug effects)
• Cell Proliferation (drug effects)
• Cyclin B1 (genetics, metabolism)
• Cyclin-Dependent Kinase Inhibitor p21 (genetics, metabolism)
• Flavonoids (pharmacology)
• G2 Phase (drug effects)
• Glioblastoma (genetics, metabolism, pathology)
• Humans
• RNA, Messenger (genetics)
• Real-Time Polymerase Chain Reaction
• Tumor Cells, Cultured
• Tumor Suppressor Protein p53 (genetics, metabolism)