Shuo Ren

Publications (2)8.86 Total impact

• Article: PI3K inhibitors changed the p53-induced response of Saos-2 cells from growth arrest to apoptosis.

  Shuo Ren, ChongFeng Gao, Lilin Zhang, Katsuro Koike, Nobuo Tsuchida
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  ABSTRACT: p53 is activated by stress leading to oncogenic alteration, which induces either cell cycle arrest or apoptosis, although the mechanism involved in this decision has not been fully clarified as yet. This work was undertaken to change the cellular response by inducing apoptosis with PI3K inhibitors to Saos-2 cells that had been growth-arrested in both G1 and G2/M by the wild-type activity of temperature-sensitive (ts) p53. We found that the PI3K/Akt inhibitors LY294002 and wortmannin, but not the MEK inhibitor U0126, were capable of inducing apoptosis in growth-arrested Saos-2 cells, as assessed by an increase in the sub-G1 population, pyknotic nuclei, and DNA ladder formation. We detected the cleavage of caspases 9 and 3, and PARP after LY294002 addition, accompanied by a loss of cytochrome c from the mitochondria, and observed Bax translocation to the mitochondria and down-regulation of phospho-Akt, suggesting that blocking of survival signals triggered the apoptotic signal through the mitochondrial apoptotic pathway. It is thus suggested that the PI3K/Akt pathway played an important role in determining cell fate between growth arrest and apoptosis.
  Biochemical and Biophysical Research Communications 09/2003; 308(1):120-5. · 2.48 Impact Factor
• Article: P130 and its truncated form mediate p53-induced cell cycle arrest in Rb(-/-) Saos2 cells.

  Chong-Feng Gao, Shuo Ren, Jingfei Wang, Sheng-Liang Zhang, Feng Jin, Takuma Nakajima, Masaaki Ikeda, Nobuo Tsuchida
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  ABSTRACT: In the present study, we investigate the mechanism of how p53 induces growth arrest in Rb-defective Saos2 cells that express temperature-sensitive mutant p53 (ts p53). The activation of p53 at a permissive temperature (32.5 degrees C) induces the cell cycle arrest at both the G1 and G2 stages. The induction of several p53-responsive genes as well as a small form of p130 (S-p130) was detected upon p53 activation. S-p130 retained the functions as a pocket protein and was dominant over p130 at the protein level after 36 h at 32.5 degrees C. A canonical p53 binding site was identified in intron 4 of p130. Furthermore, a novel p53-inducible transcript containing a partial intron 4 sequence downstream of the p53 binding site and exon 5 of p130 was detected by RT-PCR, suggesting S-p130 is induced by p53 at transcriptional level. The results from gel shift assay and immunoprecipitation showed that S-p130 as well as p130 formed complexes with both E2F1 and E2F4 at a permissive temperature. Moreover, the transient expression of E1A (12S) and E2F1 effectively abrogated p53-induced cell cycle arrest. These results strongly suggested that p130 and its truncated form might substitute Rb in mediating p53-induced cell cycle arrest in Rb(-/-) Saos2 cells.
  Oncogene 11/2002; 21(49):7569-79. · 6.37 Impact Factor