Prostate derived factor in human prostate cancer cells: Gene induction by vitamin D via a p53-dependent mechanism and inhibition of prostate cancer cell growth

2006 ◽  
Vol 208 (3) ◽  
pp. 566-574 ◽  
Author(s):  
James R. Lambert ◽  
Julie A. Kelly ◽  
Minsub Shim ◽  
William E. Huffer ◽  
Steven K. Nordeen ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Vitamin D ◽  
Cell Growth ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Prostate Cancer Cell ◽  
Human Prostate Cancer ◽  
Prostate Cancer Cells ◽  
Cancer Cell Growth ◽  
Dependent Mechanism

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 Distinct roles for the RNA-binding protein Staufen1 in prostate cancer

BMC Cancer ◽  
2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Kristen A. Marcellus ◽  
Tara E. Crawford Parks ◽  
Shekoufeh Almasi ◽  
Bernard J. Jasmin
Keyword(s):  
Prostate Cancer ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Rna Binding ◽  
Prostate Cancer Cell ◽  
Rna Binding Protein ◽  
Migration And Invasion ◽  
Human Prostate Cancer ◽  
Prostate Cancer Cells ◽  
Prostate Cells

Abstract Background Prostate cancer is one of the most common malignant cancers with the second highest global rate of mortality in men. During the early stages of disease progression, tumour growth is local and androgen-dependent. Despite treatment, a large percentage of patients develop androgen-independent prostate cancer, which often results in metastases, a leading cause of mortality in these patients. Our previous work on the RNA-binding protein Staufen1 demonstrated its novel role in cancer biology, and in particular rhabdomyosarcoma tumorigenesis. To build upon this work, we have focused on the role of Staufen1 in other forms of cancer and describe here the novel and differential roles of Staufen1 in prostate cancer. Methods Using a cell-based approach, three independent prostate cancer cell lines with different characteristics were used to evaluate the expression of Staufen1 in human prostate cancer relative to control prostate cells. The functional impact of Staufen1 on several key oncogenic features of prostate cancer cells including proliferation, apoptosis, migration and invasion were systematically investigated. Results We show that Staufen1 levels are increased in all human prostate cancer cells examined in comparison to normal prostate epithelial cells. Furthermore, Staufen1 differentially regulates growth, migration, and invasion in the various prostate cancer cells assessed. In LNCaP prostate cancer cells, Staufen1 regulates cell proliferation through mTOR activation. Conversely, Staufen1 regulates migration and invasion of the highly invasive, bone metastatic-derived, PC3 prostate cells via the activation of focal adhesion kinase. Conclusions Collectively, these results show that Staufen1 has a direct impact in prostate cancer development and further demonstrate that its functions vary amongst the prostate cancer cell types. Accordingly, Staufen1 represents a novel target for the development of much-needed therapeutic strategies for 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 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 URG11 Regulates Prostate Cancer Cell Proliferation, Migration, and Invasion

2018 ◽  
Vol 2018 ◽  
pp. 1-10 ◽  
Author(s):  
Bin Pan ◽  
Yunlin Ye ◽  
Haiping Liu ◽  
Jianli Zhen ◽  
Hongmei Zhou ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Prostate Cancer Cell ◽  
Human Prostate ◽  
Migration And Invasion ◽  
Epithelial Cell Line ◽  
Human Prostate Cancer ◽  
Prostate Cancer Cells ◽  
Colon Cancers

Upregulated gene 11 (URG11), a new gene upregulated by hepatitis B virus X protein, is involved in the development and progression of several tumors, including liver, stomach, lung, and colon cancers. However, the role of URG11 in prostate cancer remains yet to be elucidated. By determined expression in human prostate cancer tissues, URG11 was found significantly upregulated and positively correlated with the severity of prostate cancer, compared with that in benign prostatic hyperplasia tissues. Further, the mRNA and protein levels of URG11 were significantly upregulated in human prostate cancer cell lines (DU145, PC3, and LNCaP), compared with human prostate epithelial cell line (RWPE-1). Moreover, by the application of siRNA against URG11, the proliferation, migration, and invasion of prostate cancer cells were markedly inhibited. Genetic knockdown of URG11 also induced cell cycle arrest at G1/S phase, induced apoptosis, and decreased the expression level of β-catenin in prostate cancer cells. Overexpression of URG11 promoted the expression of β-catenin, the growth, the migration, and invasion ability of prostate cancer cells. Taken together, this study reveals that URG11 is critical for the proliferation, migration, and invasion in prostate cancer cells, providing the evidence of URG11 to be a novel potential therapeutic target of prostate cancer.

Suppression of human prostate cancer cell growth by forced expression of connexin genes

1999 ◽  
Vol 24 (1-2) ◽  
pp. 91-110 ◽  
Author(s):  
Parmender P. Mehta ◽  
Carlos Perez-Stable ◽  
Mehrdad Nadji ◽  
Mohsin Mian ◽  
Kamlesh Asotra ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cell Growth ◽  
Cancer Cell ◽  
Prostate Cancer Cell ◽  
Human Prostate ◽  
Human Prostate Cancer ◽  
Cancer Cell Growth ◽  
Human Prostate Cancer Cell ◽  
Connexin Genes
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