scholarly journals 15,16-Dihydrotanshinone I, a Compound ofSalvia miltiorrhizaBunge, Induces Apoptosis through Inducing Endoplasmic Reticular Stress in Human Prostate Carcinoma Cells

2011 ◽  
Vol 2011 ◽  
pp. 1-9 ◽  
Author(s):  
Mao-Te Chuang ◽  
Feng-Ming Ho ◽  
Chien-Chih Wu ◽  
Shao-Yu Zhuang ◽  
Shyr-Yi Lin ◽  
...  
Keyword(s):  
Er Stress ◽  
Prostate Carcinoma ◽  
Therapeutic Potential ◽  
Binding Protein ◽  
Salvia Miltiorrhiza ◽  
Carcinoma Cells ◽  
Initiation Factor ◽  
Human Prostate ◽  
Induced Apoptosis ◽  
Stress Dependent

5,16-dihydrotanshinone I (DHTS) is extracted fromSalvia miltiorrhizaBunge (tanshen root) and was found to be the most effective compound of tanshen extracts against breast cancer cells in our previous studies. However, whether DHTS can induce apoptosis through an endoplasmic reticular (ER) stress pathway was examined herein. In this study, we found that DHTS significantly inhibited the proliferation of human prostate DU145 carcinoma cells and induced apoptosis. DHTS was able to induce ER stress as evidenced by the upregulation of glucose regulation protein 78 (GRP78/Bip) and CAAT/enhancer binding protein homologous protein/growth arrest- and DNA damage-inducible gene 153 (CHOP/GADD153), as well as increases in phosphorylated eukaryotic initiation factor 2α (eIF2α), c-jun N-terminal kinase (JNK), and X-box-binding protein 1 (XBP1) mRNA splicing forms. DHTS treatment also caused significant accumulation of polyubiquitinated proteins and hypoxia-inducible factor (HIF)-1α, indicating that DHTS might be a proteasome inhibitor that is known to induce ER stress or enhance apoptosis caused by the classic ER stress-dependent mechanism. Moreover, DHTS-induced apoptosis was reversed by salubrinal, an ER stress inhibitor. Results suggest that DHTS can induce apoptosis of prostate carcinoma cells via induction of ER stress and/or inhibition of proteasome activity, and may have therapeutic potential for prostate cancer patients.

AN N-terminal Smac peptide sensitizes human prostate carcinoma cells to methyl jasmonate-induced apoptosis

2011 ◽  
Vol 302 (1) ◽  
pp. 37-46 ◽  
Author(s):  
Guosong Jiang ◽  
Jun Zhao ◽  
Xingyuan Xiao ◽  
Dan Tao ◽  
Chaohui Gu ◽  
...  
Keyword(s):  
Methyl Jasmonate ◽  
Prostate Carcinoma ◽  
Carcinoma Cells ◽  
Human Prostate ◽  
Human Prostate Carcinoma ◽  
Induced Apoptosis

Suppression of tumorigenicity of human prostate carcinoma cells by replacing a mutated RB gene

Science ◽  
1990 ◽  
Vol 247 (4943) ◽  
pp. 712-715 ◽  
Author(s):  
R Bookstein ◽  
J. Shew ◽  
P. Chen ◽  
P Scully ◽  
W. Lee
Keyword(s):  
Prostate Carcinoma ◽  
Carcinoma Cells ◽  
Human Prostate ◽  
Human Prostate Carcinoma ◽  
Rb Gene

scholarly journals Tubeimoside-1 induces oxidative stress-mediated apoptosis and G0/G1 phase arrest in human prostate carcinoma cells in vitro

2016 ◽  
Vol 37 (7) ◽  
pp. 950-962 ◽  
Author(s):  
Jing-bo Yang ◽  
Muhammad Khan ◽  
Yang-yang He ◽  
Min Yao ◽  
Yong-ming Li ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Prostate Carcinoma ◽  
Carcinoma Cells ◽  
Human Prostate ◽  
G1 Phase ◽  
Phase Arrest ◽  
G1 Phase Arrest ◽  
Human Prostate Carcinoma

Methylglyoxal–Induced Apoptosis in Human Prostate Carcinoma: Potential Modality for Prostate Cancer Treatment

2000 ◽  
Vol 37 (6) ◽  
pp. 728-734 ◽  
Author(s):  
Dan M. Milanesa ◽  
Muhammad S. Choudhury ◽  
Camille Mallouh ◽  
Hiroshi Tazaki ◽  
Sensuke Konno
Keyword(s):  
Prostate Cancer ◽  
Cancer Treatment ◽  
Prostate Carcinoma ◽  
Human Prostate ◽  
Prostate Cancer Treatment ◽  
Human Prostate Carcinoma ◽  
Induced Apoptosis

scholarly journals Nintedanib inhibits growth of human prostate carcinoma cells by modulating both cell cycle and angiogenesis regulators

2018 ◽  
Vol 8 (1) ◽  
Author(s):  
Raquel Frenedoso da Silva ◽  
Deepanshi Dhar ◽  
Komal Raina ◽  
Dileep Kumar ◽  
Rama Kant ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Prostate Carcinoma ◽  
Carcinoma Cells ◽  
Human Prostate ◽  
Human Prostate Carcinoma

Abstract 590: Increased Endoplasmic Reticulum Stress in Atherosclerotic Plaques Associated With Acute Coronary Syndrome

Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Masafumi Myoishi ◽  
Testuo Minamino ◽  
Masafumi Kitakaze
Keyword(s):  
Endoplasmic Reticulum ◽  
Coronary Artery ◽  
Er Stress ◽  
Atherosclerotic Plaques ◽  
Coronary Syndrome ◽  
Er Chaperone ◽  
Unstable Plaques ◽  
Induced Apoptosis ◽  
Stress Dependent ◽  
Dependent Pathway

Background Endoplasmic reticulum (ER) responds to various stresses by up-regulation of ER chaperones, and prolonged ER stress eventually causes apoptosis. Although apoptosis is considered to be essential for the progression and rupture of atherosclerotic plaques, the influence of ER stress and apoptosis on rupture of unstable coronary plaques remains unclear. Methods and Results We obtained 152 coronary artery segments at autopsy and 40 atherectomy specimens from 71 and 40 patients, respectively . Smooth muscle cells (SMCs) and macrophages in the fibrous caps of thin cap atheroma and ruptured plaques, but not in the fibrous caps of thick cap atheroma and fibrous plaques, showed a marked increase in the expression of ER chaperone and numbers of apoptotic cells. ER chaperones also expressed higher in atherectomy specimens from patients with unstable angina pectoris than with stable angina. To explore the plausible molecular mechanism of activation of ER stress and the mechanistic link to apoptosis, we investigated plaque lipids such as oxysterols. Among oxysterols, expression of 7-ketocholesterol was increased in the fibrous caps of thin cap atheroma compared with thick cap atheroma. Treatment of either cultured coronary artery SMCs or THP-1 cells with 7-ketocholesterol induced upregulation of ER chaperones and apoptosis, while these changes were prevented by antioxidants. We also investigated possible signaling pathways for ER-initiated apoptosis and found that the CHOP (a transcription factor induced by ER stress)-dependent pathway was activated in unstable plaques. In addition, knockdown of CHOP expression by siRNA decreased ER stress-dependent death of cultured coronary artery SMCs and THP-1 cells. Conclusions Increased ER stress occurs in unstable plaques. Our findings suggest that ER stress-induced apoptosis of SMCs and macrophages may contribute to plaque vulnerability.

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