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200 uM of each deoxyribonucleotide triphosphate, and 50 units/mL Super Taq DNA polymerase with the following oligonucleotide primers: 5 AACAGAGTAGCAGCTCAGACTGC 3 and 5 TCCTTCTGGGTAGACCTCTGGGAG 3. The cDNA of glyceraldehyde 3phosphate dehydrogenase Fingolimod was also amplied as a control in the same method using the following primers: Apoptotic cell death was analyzed by ow cytometry using the Annexin V conjugated Alexa Fluor 488 Apoptosis Detection Kit according the manufacturers instructions. Data are presented as the mean the standard error for the indicated number of independently performed experiments.

signals, including PERK, eIF2, and JNK, which are known to be activated in response to accumulated unfolded proteins in the ER lumen. As shown in Figure 4, DHTS indeed induced the phosphorylation of PERK, its substrate, eIF2, and JNK in dose Cell Cycle inhibitor and timedependent manners. The results suggested that DHTS is able to induce ER stress in prostate DU145 carcinoma cells. To examine whether DHTS can inhibit proteasome activity, cause ER stress, block UPR, and subsequently trigger apoptosis, lysates of cells treated with

the involvement of ER stress in the induction of apoptosis by DHTS in human prostate carcinoma cells. Abundant evidence demonstrated that androgens and the androgen receptor are associated with the development and progression of prostate pathogenesis. In addition to androgen independent DU145 cells, androgen independent PC3 cells and androgen dependent LNCaP prostate cancer cells were used to analyze the apoptotic activity of DHTS. Our results indicated that DHTS signicantly inhibited both the proliferation of androgen dependent LNCaP and androgen independent PC3 and DU145 cells in the same manner, suggesting that the antiproliferative NSCLC eects of DHTS are not irrelevant to the androgen signal pathway. Reactive oxygen species are known to inhibit ER calcium pumps and ultimately result in depletion of ER calcium stores. The shortage of ER calcium causes a deterioration in the proper folding of proteins in the lumen of the ER and causes ER stress. In this study, we found that DHTS signicantly induced ER stress, such as upregulation of GRP78/Bip and CHOP/GADD153 protein expressions and PERK, eIF2, and JNK phosphorylation. Other studies demonstrated that tanshinones,