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 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.

scholarly journals Molecular signatures associated with prostate cancer cell line (PC-3) exposure to inactivated Zika virus

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Jeany Delafiori ◽  
Estela de Oliveira Lima ◽  
Mohamed Ziad Dabaja ◽  
Flávia Luísa Dias-Audibert ◽  
Diogo Noin de Oliveira ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cell Growth ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Zika Virus ◽  
Prostate Cancer Cell ◽  
Antiproliferative Effect ◽  
Mass Spectrometry Analysis ◽  
Molecular Signatures ◽  
Prostate Cancer Cells

Abstract The recent outbreak of Zika virus (ZIKV) infection associated with microcephaly cases has elicited much research on the mechanisms involved in ZIKV-host cell interactions. It has been described that Zika virus impairs cell growth, raising a hypothesis about its oncolytic potential against cancer cells. ZIKV tumor cell growth inhibition was later confirmed for glioblastoma. It was also demonstrated that an inactivated ZIKV prototype (ZVp) based on bacterial outer membrane vesicles has antiproliferative activity upon other cancer cell lines, such as PC-3 prostate cancer cell. This study aims at understanding the pathways that might be involved with the antiproliferative effect of Zika virus against prostate cancer cells. A metabolomic approach based on high-resolution mass spectrometry analysis led to the identification of 21 statistically relevant markers of PC-3 cells treated with ZVp. The markers were associated with metabolic alterations that trigger lipid remodeling, endoplasmic reticulum stress, inflammatory mediators, as well as disrupted porphyrin and folate metabolism. These findings highlight molecular signatures of ZVp-induced response that may be involved on cellular pathways triggered by its antiproliferative effect. To our knowledge, this is the first reported metabolomic assessment of ZIKV effect on prostate cancer cells, a promising topic for further research.

scholarly journals Regulation of Expression of Deoxyhypusine Hydroxylase (DOHH), the Enzyme That Catalyzes the Activation of eIF5A, by miR-331-3p and miR-642-5p in Prostate Cancer Cells

2012 ◽  
Vol 287 (42) ◽  
pp. 35251-35259 ◽  
Author(s):  
Michael R. Epis ◽  
Keith M. Giles ◽  
Felicity C. Kalinowski ◽  
Andrew Barker ◽  
Ronald J. Cohen ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cell Growth ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Prostate Cancer Cell ◽  
Translation Initiation Factor ◽  
Initiation Factor ◽  
Prostate Cancer Cells ◽  
Normal Prostate ◽  
Deoxyhypusine Hydroxylase

The enzyme deoxyhypusine hydroxylase (DOHH) catalyzes the activation of eukaryotic translation initiation factor (eIF5A), a protein essential for cell growth. Using bioinformatic predictions and reporter gene assays, we have identified a 182-nt element within the DOHH 3′-untranslated region (3′-UTR) that contains a number of target sites for miR-331-3p and miR-642-5p. Quantitative RT-PCR studies demonstrated overexpression of DOHH mRNA and underexpression of miR-331-3p and miR-642-5p in several prostate cancer cell lines compared with normal prostate epithelial cells. Transient overexpression of miR-331-3p and/or miR-642-5p in DU145 prostate cancer cells reduced DOHH mRNA and protein expression and inhibited cell proliferation. We observed synergistic growth inhibition with the combination of miR-331-3p and miR-642-5p and mimosine, a pharmacological DOHH inhibitor. Finally, we identified a significant inverse relationship between the expression of miR-331-3p or miR-642-5p and DOHH in a cohort of human prostate cancer tissues. Our results suggest a novel role for miR-331-3p and miR-642-5p in the control of prostate cancer cell growth via the regulation of DOHH expression and eIF5A activity.

scholarly journals Knocking down claudin receptors leads to a decrease in prostate cancer cell migration, cell growth, cell viability and clonogenic cell survival

2021 ◽  
Vol 2 (1) ◽  
Author(s):  
Qiang Liu ◽  
Hongliang Shen ◽  
Andrew Naguib ◽  
Robert M. Weiss ◽  
Darryl T. Martin
Keyword(s):  
Prostate Cancer ◽  
Cell Migration ◽  
Cell Growth ◽  
Cancer Cell ◽  
Prostate Cancer Cell ◽  
Human Prostate ◽  
Human Prostate Cancer ◽  
Lncap Cells ◽  
Prostate Cancer Cells ◽  
Cancer Cell Growth

AbstractProstate cancer is the most common solid organ malignancy in the United States, and has the highest probability of all cancers in becoming invasive. New molecular targets are needed to define and impede the growth and progression of advanced prostate cancers. Claudins (Cldns) are transmembrane proteins that regulate paracellular permeability and cell polarity, and their levels are elevated in many human cancers such as breast, ovarian, pancreatic, and prostatic cancers. Previously, we found that Cldn3 and Cldn4 are expressed in aggressive high-grade human prostate cancer specimens. We and others have shown that there are higher levels of Cldn3 and Cldn4 in metastatic human prostate cancer cells than in normal human prostate cells. The result of targeting Cldn3 and Cldn4 expression on the growth and viability of prostate cancer cells has not been elucidated. Human prostate cancer PC3 and LNCaP cells were transfected with Cldn3 or -4 small interfering RNAs (siRNAs). Cldn3/Cldn4 siRNA treatment resulted in a greater than 85% decrease in the protein levels of Cldn3 and Cldn4, which was accompanied by a 30–40% decrease in prostate cancer cell growth and a 60–65% reduction in cell viability. There was decreased cell migration with Cldn3 and Cldn4 siRNA in both PC3 and LNCaP cells and a 60–75% decrease in the number of clones when treated with siCldn3 or siCldn4 compared to control. Knocking down Cldn3/Cldn4 affects prostate cancer cell growth and survival and may have therapeutic implications.

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.

794: Valproic Acid Inhibits Prostate Cancer Cell Growth in Vitro and in Vivo

2006 ◽  
Vol 175 (4S) ◽  
pp. 257-257
Author(s):  
Jennifer Sung ◽  
Qinghua Xia ◽  
Wasim Chowdhury ◽  
Shabana Shabbeer ◽  
Michael Carducci ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Valproic Acid ◽  
Cell Growth ◽  
Cancer Cell ◽  
Prostate Cancer Cell ◽  
Cancer Cell Growth
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