scholarly journals The Effect of Ethanol Baneh Skin Extract on the Expressions of Bcl - 2, Bax, and Caspase - 3 Concentration in Human Prostate Cancer pc3 Cells

2018 ◽  
Vol 11 (3) ◽  
Author(s):  
Maryam Amiri ◽  
Foad Nasrollahi ◽  
Siamak Barghi ◽  
Nazanin Ebrahimi ◽  
Afsaneh Rajizadeh ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Caspase 3 ◽  
Human Prostate ◽  
Skin Extract ◽  
Human Prostate Cancer ◽  
Pc3 Cells

scholarly journals Cytotoxic Effects of the Ethanol Bane Skin Extract in Human Prostate Cancer Pc3 Cells

2016 ◽  
Vol In Press (In Press) ◽  
Author(s):  
Maryam Amiri ◽  
Faranak Kazerouni ◽  
Saeed Namaki ◽  
Hassan Darbandi Tamijani ◽  
Hooman Rahimipour ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Human Prostate ◽  
Skin Extract ◽  
Human Prostate Cancer ◽  
Cytotoxic Effects ◽  
Pc3 Cells

Allyl Isothiocyanate Induces Autophagy through the Up-Regulation of Beclin-1 in Human Prostate Cancer Cells

2018 ◽  
Vol 46 (07) ◽  
pp. 1625-1643 ◽  
Author(s):  
Hung-En Chen ◽  
Ji-Fan Lin ◽  
Te-Fu Tsai ◽  
Yi-Chia Lin ◽  
Kuang-Yu Chou ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cancer Cells ◽  
Allyl Isothiocyanate ◽  
Beclin 1 ◽  
Human Prostate ◽  
Human Prostate Cancer ◽  
Prostate Cancer Cells ◽  
Normal Prostate ◽  
Autophagy Induction ◽  
Pc3 Cells

Allyl isothiocyanate (AITC), one of the most widely studied phytochemicals, inhibits the survival of human prostate cancer cells while minimally affecting normal prostate epithelial cells. Our study demonstrates the mechanism of AITC-induced cell death in prostate cancer cells. AITC induces autophagy in RV1 and PC3 cells, judging from the increased level of LC3-II protein in a dose- and time-dependent manner, but not in the normal prostate epithelial cell (PrEC). Inhibition of autophagy in AITC-treated cells decreased cell viability and enhanced apoptosis, suggesting that the autophagy played a protective role. There are several pathways activated in ATIC-treated cells. We detected the phosphorylation forms of mTOR, ERK, AMPK, JNK and p38, and ERK AMPK and JNK activation were also detected. However, inhibition of AITC-activated ERK, AMPK and JNK by pre-treatment of specific inhibitors did not alter autophagy induction. Finally, increased beclin-1 expression was detected in AITC-treated cells, and inhibition of AITC-induced beclin-1 attanuated autophagy induction, indicating that AITC-induced autophagy occurs through upregulating beclin-1. Overall, our data show for the first time that AITC induces protective autophagy in Rv1 and PC3 cells through upregulation of beclin-1. Our results could potentially contribute to a therapeutic application of AITC in prostate cancer patients.

Inhibition of PARP1 by small interfering RNA enhances docetaxel activity against human prostate cancer PC3 cells

2013 ◽  
Vol 442 (1-2) ◽  
pp. 127-132 ◽  
Author(s):  
Wenqi Wu ◽  
Zhenzhen Kong ◽  
Xiaolu Duan ◽  
Hanliang Zhu ◽  
Shujue Li ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Small Interfering Rna ◽  
Human Prostate ◽  
Human Prostate Cancer ◽  
Pc3 Cells ◽  
Interfering Rna

scholarly journals Inhibition of Prostate Cancer Cell Growth by Human Secreted PDZ Domain-Containing Protein 2, a Potential Autocrine Prostate Tumor Suppressor

Endocrinology ◽  
2006 ◽  
Vol 147 (11) ◽  
pp. 5023-5033 ◽  
Author(s):  
C. W. Tam ◽  
A. S. Cheng ◽  
R. Y. M. Ma ◽  
K.-M. Yao ◽  
S. Y. W. Shiu
Keyword(s):  
Prostate Cancer ◽  
Cancer Cells ◽  
Caspase 3 ◽  
Pdz Domain ◽  
Human Prostate ◽  
Human Prostate Cancer ◽  
Lncap Cells ◽  
Prostate Cancer Cells ◽  
Autocrine Growth ◽  
Endogenous Expression

A possible role of the PDZ domain-containing protein 2 (PDZD2) in prostate tumorigenesis has been suggested. Besides, PDZD2 is posttranslationally cleaved by a caspase-dependent mechanism to form a secreted PDZ domain-containing protein 2 (sPDZD2) with unknown functions in humans. In this study, we demonstrate the endogenous expression of PDZD2 and secretion of sPDZD2 in cancerous DU145, PC-3, 22Rv1, LNCaP, and immortalized RWPE-1 prostate epithelial cells. Inhibition of endogenous sPDZD2 production and secretion by DU145, PC-3, 22Rv1, and RWPE-1 cells via the caspase-3 inhibitor Z-DEVD-FMK resulted in increased cell proliferation, which was abrogated by treatment with exogenous recombinant sPDZD2. Whereas sPDZD2-induced antiproliferation in DU145, PC-3, and 22Rv1 cells, it induced apoptosis in LNCaP cells. The data suggest that endogenous sPDZD2, produced by caspase-3-mediated cleavage from PDZD2, may function as a novel autocrine growth suppressor for human prostate cancer cells. The antiproliferative effect of sPDZD2 was apparently mediated through slowing the entry of DU145, PC-3, and 22Rv1 cells into the S phase of the cell cycle. In DU145 cells, this can be attributed to stimulated p53 and p21CIP1/WAF1 expression by sPDZD2. On the other hand, the apoptotic effect of sPDZD2 on LNCaP cells was apparently mediated via p53-independent Bad stimulation. Together our results indicate the presence of p53-dependent and p53-independent PDZD2/sPDZD2 autocrine growth suppressive signaling pathways in human prostate cancer cells and suggest a novel therapeutic approach of harnessing the latent tumor-suppressive potential of an endogenous autocrine signaling protein like sPDZD2 to inhibit prostate cancer growth.

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