EGCG inhibits protein synthesis, lipogenesis, and cell cycle progression through activation of AMPK in p53 positive and negative human hepatoma cells

2009 ◽  
Vol 53 (9) ◽  
pp. 1156-1165 ◽  
Author(s):  
Chi-Hung Huang ◽  
Shang-Jie Tsai ◽  
Ying-Jan Wang ◽  
Min-Hsiung Pan ◽  
Jung-Yie Kao ◽  
...  
1992 ◽  
Vol 263 (5) ◽  
pp. H1331-H1338 ◽  
Author(s):  
T. Nagata ◽  
Y. Uehara ◽  
A. Numabe ◽  
T. Ishimitsu ◽  
N. Hirawa ◽  
...  

We investigated the regulatory effects of the vasoconstrictor thromboxane A2 on the proliferation of vascular smooth muscle cells (VSMC) from Wistar-Kyoto rats using 9,11-epithio-11,12-methano-thromboxane A2 (STA2), a stable analogue of thromboxane A2. STA2 dose dependently increased incorporation of [3H]thymidine into DNA in randomly cycling VSMC and significantly shortened the doubling time. Cell cycle analysis revealed that the increased cell cycle progression was primarily due to a rapid transition from the DNA synthetic (S) to the G2/mitotic (M) phase. Moreover, STA2 enhanced protein synthesis in VSMC during the G2/M phase, whereas the protein synthesis was unaffected in the G0/G1 period. In fact, STA2 prompted the cells in G2/M phase to synthesize actin, a major cytoskeleton protein. Conversely, inhibition of protein synthesis by puromycin retarded the transition from S to G2/M. In addition, depolymerization of the actin molecules by cytochalasin D offset the quick progression to the G2/M phase by STA2. These data indicate that thromboxane A2 stimulates the cell cycle progression in VSMC primarily through a rapid transition from S to G2/M. This enhanced progression is attributable partly to a rapid buildup of the cytoskeleton proteins during the G2/M period.


2012 ◽  
Vol 365 (1) ◽  
pp. 303-309 ◽  
Author(s):  
Vlad Costache ◽  
Stefania Bilotto ◽  
Laurent Laguerre ◽  
Robert Bellé ◽  
Bertrand Cosson ◽  
...  

1993 ◽  
Vol 106 (1) ◽  
pp. 299-307
Author(s):  
O. Larsson ◽  
M. Carlberg ◽  
A. Zetterberg

Treatment with a low dose (0.5 microgram/ml) of tunicamycin (an inhibitor of N-linked glycosylation) blocked the cell cycle progression of both normal Balb/c 3T3 cells (A31) and their SV40-transformed derivatives (SVA31) specifically in early G1 (0-3 h after mitosis). Upon release after an 8-h treatment the A31 cells returned to the cell cycle via a 9-h recovery phase, indicating that they were arrested in G0. The A31 cells were fully viable after this treatment. In contrast, the postmitotic SVA31 cells, which were unable to arrest in G0, did not divide after the removal of tunicamycin. Instead, these cells died but this did not occur until 22–34 h after release from the treatment. SVA31 cells that had passed the postmitotic phase of G1 survived during the parental generation and divided normally. However, a large portion of these cells died during the next cycle, and in total during a 48-h period approximately 50% of the cells were killed as a consequence of an 8-h exposure to tunicamycin. In contrast, treatment with inhibitors of protein synthesis and HMG CoA reductase activity as well as inhibitors of modification of N-linked oligosaccharide chains did not result in cell death.


2008 ◽  
Vol 29 (12) ◽  
pp. 2279-2288 ◽  
Author(s):  
Andrea Bianchini ◽  
Maria Loiarro ◽  
Pamela Bielli ◽  
Roberta Busà ◽  
Maria Paola Paronetto ◽  
...  

Sign in / Sign up

Export Citation Format

Share Document