scholarly journals Inhibition of Recombining Binding Protein Suppressor of Hairless (RBPJ) Impairs the Growth of Prostate Cancer

2015 ◽  
Vol 36 (5) ◽  
pp. 1982-1990 ◽  
Author(s):  
Li Xue ◽  
Hecheng Li ◽  
Qi Chen ◽  
Zhenlong Wang ◽  
Peng Zhang ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cell Cycle ◽  
Cell Growth ◽  
Cancer Cells ◽  
Receptor Activation ◽  
Notch Signaling Pathway ◽  
Notch Receptor ◽  
Prostate Cancer Cells ◽  
Cancer Cell Growth ◽  
Promising Therapeutic Approach

Background/Aims: Notch signaling pathway regulates cancer cell growth. RBPJ is a key transcription factor downstream of Notch receptor activation, whereas the role of RBPJ in carcinogenesis of prostate cancer is ill-defined. Methods: Here, we evaluated the effects of RBPJ inhibition on the growth of prostate cancer cells. We knocked down RBPJ in prostate cancer cells by a short hairpin interfering RNA (shRNA). We measured cell growth by an MTT assay. We analyzed the levels of cell-cycle-associated proteins by Western blot. Results: We found that shRNA for RBPJ efficiently inhibited RBPJ expression in prostate cancer cells, resulting in a significant decrease in the cell growth. Further, RBPJ-mediated cell-growth inhibition appeared to be resulting from alteration of cell-cycle inhibitors p21 and p27, cell-cycle activators CDK2, CDK4 and CyclinD1, and apoptosis-suppressor Bcl-2. Conclusion: Our data suggest that shRNA intervention of RBPJ expression could be a promising therapeutic approach for treating human prostate cancer.

Material properties of disulfide-crosslinked hyaluronic acid hydrogels influence prostate cancer cell growth and metabolism

2020 ◽  
Vol 8 (42) ◽  
pp. 9718-9733
Author(s):  
Nicky W. Tam ◽  
Dudley Chung ◽  
Samuel J. Baldwin ◽  
Jeffrey R. Simmons ◽  
Lingling Xu ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Hyaluronic Acid ◽  
Cell Growth ◽  
Cancer Cells ◽  
Material Properties ◽  
Prostate Cancer Cell ◽  
Prostate Cancer Cells ◽  
Cancer Cell Growth ◽  
Diffusion Limited ◽  
Metastatic Cells

Studying prostate cancer cells embedded in hyaluronic acid hydrogels provides insight on how metastatic cells might behave in diffusion-limited tissue microenvironments.

scholarly journals Traditional Herbal Formula Taeeumjowi-Tang (TJ001) Inhibits p53-Mutant Prostate Cancer Cells Growth by Activating AMPK-Dependent Pathway

2019 ◽  
Vol 2019 ◽  
pp. 1-11 ◽  
Author(s):  
Sooyeon Kang ◽  
Hyo In Kim ◽  
Yu-Jeong Choi ◽  
Seul Ki Lee ◽  
Ji Hye Kim ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cell Cycle ◽  
Cell Growth ◽  
Cell Cycle Arrest ◽  
Cancer Cells ◽  
Caspase 3 ◽  
Mutant P53 ◽  
Prostate Cancer Cells ◽  
Cycle Arrest ◽  
Du145 Cells

Dysregulated lipid metabolism is a prominent feature of prostate cancers (PCas); several enzymes involved in lipid accumulation are highly expressed. Here, we elucidated efficacy of TJ001, a traditional herbal decoction, in inhibiting de novo lipogenesis. TJ001 had significant cytotoxicity against DU145 but not PC3 and LNCaP cells and, similarly, TJ001 markedly AMPK phosphorylation only in DU145 cells. This was accompanied by the downregulation of phosphorylated-acetyl coenzyme A carboxylase (ACC) expression and sterol regulatory element-binding protein 1 (SREBP1) proteolytic cleavage, thereby inhibiting its role as a transcription factor to induce lipid biosynthesis. When Oil Red O staining was performed, it is reflected in the reduction of lipid droplets (LDs). TJ001 also induced G1/S cell cycle arrest via a cell cycle inhibitor (CKI) p21WAF1/CIP1 upregulation. Although p53 proteins remained unchanged, both cyclin E and cyclin D1 were decreased. Moreover, TJ001 suppressed the mammalian target of rapamycin (mTOR) signaling pathway. Generally, the prolonged G1/S phase arrest accompanies apoptosis, but TJ001 failed to work as a trigger apoptosis in DU145 cells. We showed that mutant p53 proteins were required for the survival of DU145 cells. In presence of TJ001, inhibition of endogenous mutant p53 by RNAi led to cell viability reduction and induction of the p-AMPK/AMPK ratio. In addition, it induced apoptotic cell death in DU145 cells. At the cellular level, induction of PARP, caspase-3, and caspase-9 cleavages was observed, and caspase-3 activity was increased in the p53 knockdown cells treated with TJ001. Taken together, we demonstrated that TJ001 inhibited cell growth in DU145 prostate cancer cells as indicated by blocking lipogenesis and induction in G1/S cell cycle arrest. In addition, we may provide an evidence that mutant p53 protein has potential role as an oncogenic action in DU145 cells. Collectively, the combination of mutant p53 targeting and TJ001 treatment resulted in decreased cell growth in DU145 cells.

scholarly journals Indole-3-carbinol (I3C) induced cell growth inhibition, G1 cell cycle arrest and apoptosis in prostate cancer cells

Oncogene ◽  
2001 ◽  
Vol 20 (23) ◽  
pp. 2927-2936 ◽  
Author(s):  
Sreenivasa R Chinni ◽  
Yiwei Li ◽  
Sunil Upadhyay ◽  
Prathima K Koppolu ◽  
Fazlul H Sarkar
Keyword(s):  
Prostate Cancer ◽  
Cell Cycle ◽  
Cell Growth ◽  
Growth Inhibition ◽  
Cell Cycle Arrest ◽  
Cancer Cells ◽  
Cell Growth Inhibition ◽  
Prostate Cancer Cells ◽  
Cycle Arrest ◽  
G1 Cell Cycle Arrest

scholarly journals The Steroidogenic Enzyme AKR1C3 Regulates Stability of the Ubiquitin Ligase Siah2 in Prostate Cancer Cells

2015 ◽  
Vol 290 (34) ◽  
pp. 20865-20879 ◽  
Author(s):  
Lingling Fan ◽  
Guihong Peng ◽  
Arif Hussain ◽  
Ladan Fazli ◽  
Emma Guns ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cell Growth ◽  
Cancer Cells ◽  
Ubiquitin Ligase ◽  
Castration Resistant Prostate Cancer ◽  
Prostate Cancer Cells ◽  
Cancer Cell Growth ◽  
Protein Levels ◽  
Castration Resistant

Re-activation of androgen receptor (AR) activity is the main driver for development of castration-resistant prostate cancer. We previously reported that the ubiquitin ligase Siah2 enhanced AR transcriptional activity and prostate cancer cell growth. Among the genes we found to be regulated by Siah2 was AKR1C3, which encodes a key androgen biosynthetic enzyme implicated in castration-resistant prostate cancer development. Here, we found that Siah2 inhibition in CWR22Rv1 prostate cancer cells decreased AKR1C3 expression as well as intracellular androgen levels, concomitant with inhibition of cell growth in vitro and in orthotopic prostate tumors. Re-expression of either wild-type or catalytically inactive forms of AKR1C3 partially rescued AR activity and growth defects in Siah2 knockdown cells, suggesting a nonenzymatic role for AKR1C3 in these outcomes. Unexpectedly, AKR1C3 re-expression in Siah2 knockdown cells elevated Siah2 protein levels, whereas AKR1C3 knockdown had the opposite effect. We further found that AKR1C3 can bind Siah2 and inhibit its self-ubiquitination and degradation, thereby increasing Siah2 protein levels. We observed parallel expression of Siah2 and AKR1C3 in human prostate cancer tissues. Collectively, our findings identify a new role for AKR1C3 in regulating Siah2 stability and thus enhancing Siah2-dependent regulation of AR activity in prostate cancer cells.

Silibinin Inhibits Cell Growth and Induces Apoptosis through Cell-cycle Arrest in PC-3 Prostate Cancer Cells

2011 ◽  
Vol 21 (11) ◽  
pp. 1573-1578 ◽  
Author(s):  
Sang-Hun Kim ◽  
Kwang-Youn Kim ◽  
Sun-Nyoung Yu ◽  
Hyun-Joo Jeon ◽  
Young-Rang Jin ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cell Cycle ◽  
Cell Growth ◽  
Cell Cycle Arrest ◽  
Cancer Cells ◽  
Prostate Cancer Cells ◽  
Cycle Arrest
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