Activation of JNK by TPA promotes apoptosis via PKC pathway in gastric cancer cells

Figure 1 Expression of JNK protein in response to TPA induction. Cells treated with TPA for different time indicated. Expression of JNK protein was detected by Western blot. Amount of protein used in each lane was indicated by stain-ing with ponceau S. The intensity of each band was quantified by densitometer.

Figure 2 Expression of c-jun mRNA in response to TPA induction. Cells treated with TPA for different time indicated. Expression of c-jun mRNA was revealed by Northern blot. The same membrane was probed again with β-actin cDNA to show the amount of RNA used in each well. The intensity of each band was quantified by densitometer.

Figure 3 Effect of TPA on transcriptional activity of activator protein-1. Cells were treated with various concentrations of TPA indicated. Various expression vectors were transfected into cells as described in materials and methods. Transcrip-tional activity was measured by the method of transient trans-fection and CAT assay. Data shown represent mean of dupli-cate experiments (± SE).

Figure 4 Effect of various agents, including Wortmannin (shown by Wort. or W), a PKC specific inhibitor, on expres-sion of JNK protein. Cells were treated with Wortmannin for 2 hr, following by TPA induction for another 3 hr. Protein was detected by Western blot. Amount of protein used in each lane was indicated by staining with ponceau S. The intensity of each band was quantified by densitometer.

Figure 5 Effect of various agents, including TPA and Wortmannin, on apoptosis induction. Cells were treated with TPA and/or Wortmannin for different time indicated, and then the apoptotic rate was analyzed as described in material and methods. (A) The morphological changes in nucleus in re-sponse to different agents. (B) Apoptosis index.