Down-regulation of CEACAM1 in human prostate cancer: Correlation with loss of cell polarity, increased proliferation rate, and Gleason grade 3 to 4 transition

2002 ◽  
Vol 33 (3) ◽  
pp. 290-298 ◽  
Author(s):  
Christer Busch ◽  
Tor Arne Hanssen ◽  
Christoph Wagener ◽  
Björn Öbrink
Keyword(s):  
Prostate Cancer ◽  
Cell Polarity ◽  
Proliferation Rate ◽  
Human Prostate ◽  
Gleason Grade ◽  
Human Prostate Cancer ◽  
Down Regulation ◽  
Grade 3

Increased expression of δ-catenin/neural plakophilin-related armadillo protein is associated with the down-regulation and redistribution of E-cadherin and p120ctn in human prostate cancer

2005 ◽  
Vol 36 (10) ◽  
pp. 1037-1048 ◽  
Author(s):  
Qun Lu ◽  
Larry J. Dobbs ◽  
Christopher W. Gregory ◽  
George W. Lanford ◽  
Monica P. Revelo ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Human Prostate ◽  
Human Prostate Cancer ◽  
Down Regulation ◽  
E Cadherin

scholarly journals Sanggenol L Induces Apoptosis and Cell Cycle Arrest via Activation of p53 and Suppression of PI3K/Akt/mTOR Signaling in Human Prostate Cancer Cells

Nutrients ◽  
2020 ◽  
Vol 12 (2) ◽  
pp. 488 ◽  
Author(s):  
Yeong-Seon Won ◽  
Kwon-Il Seo
Keyword(s):  
Prostate Cancer ◽  
Cell Cycle ◽  
Cell Cycle Arrest ◽  
Cancer Cells ◽  
Mtor Signaling ◽  
Human Prostate ◽  
Human Prostate Cancer ◽  
Prostate Cancer Cells ◽  
Down Regulation ◽  
Cycle Arrest

Prostate cancer is the most common cancer in Western countries. Recently, Asian countries are being affected by Western habits, which have had an important role in the rapid increase in cancer incidence. Sanggenol L (San L) is a natural flavonoid present in the root barks of Morus alba, which induces anti-cancer activities in ovarian cancer cells. However, the molecular and cellular mechanisms of the effects of sanggenol L on human prostate cancer cells have not been elucidated. In this study, we investigated whether sanggenol L exerts anti-cancer activity in human prostate cancer cells via apoptosis and cell cycle arrest. Sanggenol L induced caspase-dependent apoptosis (up-regulation of PARP and Bax or down-regulation of procaspase-3, -8, -9, Bid, and Bcl-2), induction of caspase-independent apoptosis (up-regulation of AIF and Endo G on cytosol), suppression of cell cycle (down-regulation of CDK1/2, CDK4, CDK6, cyclin D1, cyclin E, cyclin A, and cyclin B1 or up-regulation of p53 and p21), and inhibition of PI3K/Akt/mTOR signaling (down-regulation of PI3K, p-Akt, and p-mTOR) in prostate cancer cells. These results suggest the induction of apoptosis via suppression of PI3K/Akt/mTOR signaling and cell cycle arrest via activation of p53 in response to sanggenol L in prostate cancer cells.

Down-regulation of Hsp27 radiosensitizes human prostate cancer cells

2006 ◽  
Vol 13 (9) ◽  
pp. 1221-1225 ◽  
Author(s):  
SHAHRAM TEIMOURIAN ◽  
RAZIEH JALAL ◽  
MOSTAFA SOHRABPOUR ◽  
BAHRAM GOLIAEI
Keyword(s):  
Prostate Cancer ◽  
Cancer Cells ◽  
Human Prostate ◽  
Human Prostate Cancer ◽  
Prostate Cancer Cells ◽  
Down Regulation

scholarly journals Cathepsin E enhances anticancer activity of doxorubicin on human prostate cancer cells showing resistance to TRAIL-mediated apoptosis

2010 ◽  
Vol 391 (8) ◽  
Author(s):  
Atsushi Yasukochi ◽  
Tomoyo Kawakubo ◽  
Seiji Nakamura ◽  
Kenji Yamamoto
Keyword(s):  
Prostate Cancer ◽  
Tumor Cell ◽  
Cancer Cell ◽  
Prostate Cancer Cell ◽  
Human Prostate ◽  
Human Prostate Cancer ◽  
Down Regulation ◽  
Cathepsin E

Abstract We previously described that cathepsin E specifically induces growth arrest and apoptosis in several human prostate cancer cell lines in vitro by catalyzing the proteolytic release of soluble tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) from the tumor cell surface. It also prevents tumor growth and metastasis in vivo through multiple mechanisms, including induction of apoptosis, angiogenesis inhibition and enhanced immune responses. Using the prostate cancer cell line PPC-1, which is relatively resistant to cell death by doxorubicin (40–50% cytotoxicity), we first report that a combination treatment with cathepsin E can overcome resistance of the cells to this agent. In vitro studies showed that combined treatment of PPC-1 cells with the two agents synergistically induces viability loss, mainly owing to down-regulation of a short form of the FLICE inhibitory protein FLIP. The enhanced antitumor activity was corroborated by in vivo studies with athymic mice bearing PPC-1 xenografts. Intratumoral application of cathepsin E in doxorubicin-treated mice results in tumor cell apoptosis and tumor regression in xenografts by enhanced TRAIL-induced apoptosis through doxorubicin-induced c-FLIP down-regulation and by a decrease in tumor cell proliferation. These results indicate that combination of cathepsin E and doxorubicin is sufficient to overcome resistance to TRAIL-mediated apoptosis in chemoresistant prostate cancer PPC-1 cells, thus indicating therapeutic potential for clinical use.

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