scholarly journals 345. Initial Use of Vesicular Stomatitis Virus to Differentially Kill Prostate Cancer Cells Versus Prostate Epithelial Cells

2003 ◽  
Vol 7 (5) ◽  
pp. S135
Keyword(s):  
Prostate Cancer ◽  
Epithelial Cells ◽  
Cancer Cells ◽  
Vesicular Stomatitis Virus ◽  
Prostate Cancer Cells ◽  
Prostate Epithelial Cells ◽  
Vesicular Stomatitis

Basal prostate epithelial cells stimulate the migration of prostate cancer cells

2004 ◽  
Vol 41 (2) ◽  
pp. 85-97 ◽  
Author(s):  
Hsiao-Man Yu ◽  
Diane E. Frank ◽  
Jie Zhang ◽  
Xueke You ◽  
William G. Carter ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Epithelial Cells ◽  
Cancer Cells ◽  
Prostate Cancer Cells ◽  
Prostate Epithelial Cells

scholarly journals MAP3K7 and CHD1 Are Novel Mediators of Resistance to Oncolytic Vesicular Stomatitis Virus in Prostate Cancer Cells

2020 ◽  
Vol 17 ◽  
pp. 496-507
Author(s):  
Robert S. Bayne ◽  
Shelby Puckett ◽  
Lindsey Ulkus Rodrigues ◽  
Scott D. Cramer ◽  
Jingyun Lee ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cancer Cells ◽  
Vesicular Stomatitis Virus ◽  
Prostate Cancer Cells ◽  
Vesicular Stomatitis

scholarly journals SIRT1 Modulates the Sensitivity of Prostate Cancer Cells to Vesicular Stomatitis Virus Oncolysis

2019 ◽  
Vol 93 (15) ◽  
Author(s):  
Michela Muscolini ◽  
Luciano Castiello ◽  
Enrico Palermo ◽  
Alessandra Zevini ◽  
Matteo Ferrari ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cancer Cells ◽  
Histone Deacetylase ◽  
Cancer Cell ◽  
Vesicular Stomatitis Virus ◽  
Oncolytic Virus ◽  
Prostate Cancer Cells ◽  
Intrinsic Resistance ◽  
Primary Tumors ◽  
Vesicular Stomatitis

ABSTRACT Oncolytic virotherapy represents a promising experimental anticancer strategy, based on the use of genetically modified viruses to selectively infect and kill cancer cells. Vesicular stomatitis virus (VSV) is a prototypic oncolytic virus (OV) that induces cancer cell death through activation of the apoptotic pathway, although intrinsic resistance to oncolysis is found in some cell lines and many primary tumors, as a consequence of residual innate immunity to the virus. In the effort to improve OV therapeutic efficacy, we previously demonstrated that different agents, including histone deacetylase inhibitors (HDIs), functioned as reversible chemical switches to dampen the innate antiviral response and improve the susceptibility of resistant cancer cells to VSV infection. In the present study, we demonstrated that the NAD+-dependent histone deacetylase SIRT1 (silent mating type information regulation 2 homolog 1) plays a key role in the permissivity of prostate cancer PC-3 cells to VSVΔM51 replication and oncolysis. HDI-mediated enhancement of VSVΔM51 infection and cancer cell killing directly correlated with a decrease of SIRT1 expression. Furthermore, pharmacological inhibition as well as silencing of SIRT1 by small interfering RNA (siRNA) was sufficient to sensitize PC-3 cells to VSVΔM51 infection, resulting in augmentation of virus replication and spread. Mechanistically, HDIs such as suberoylanilide hydroxamic acid (SAHA; Vorinostat) and resminostat upregulated the microRNA miR-34a that regulated the level of SIRT1. Taken together, our findings identify SIRT1 as a viral restriction factor that limits VSVΔM51 infection and oncolysis in prostate cancer cells. IMPORTANCE The use of nonpathogenic viruses to target and kill cancer cells is a promising strategy in cancer therapy. However, many types of human cancer are resistant to the oncolytic (cancer-killing) effects of virotherapy. In this study, we identify a host cellular protein, SIRT1, that contributes to the sensitivity of prostate cancer cells to infection by a prototypical oncolytic virus. Knockout of SIRT1 activity increases the sensitivity of prostate cancer cells to virus-mediated killing. At the molecular level, SIRT1 is controlled by a small microRNA termed miR-34a. Altogether, SIRT1 and/or miR-34a levels may serve as predictors of response to oncolytic-virus therapy.

MicroRNA-501-5p Targets PINX1 Gene to Regulate the Proliferation, Migration, and Invasion of Prostatic Carcinoma Cells

2021 ◽  
Vol 11 (3) ◽  
pp. 471-477
Author(s):  
Yueguang Zhao ◽  
Xiaohua Zhang ◽  
Hao Ye ◽  
Zhixian Yu ◽  
Junhua Zhu ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Epithelial Cells ◽  
Cancer Cells ◽  
Inhibitory Effect ◽  
Migration And Invasion ◽  
Prostate Cancer Cells ◽  
Normal Prostate ◽  
Prostate Epithelial Cells ◽  
Du145 Cells ◽  
High Level

The expression of PINX1 is decreased in prostate cancer, and the high level of miRNA-501-5p promotes the proliferation of liver cancer cells. However, there is no relevant research on miRNA-501-5p in prostate cancer. miRNA-501-5p can target the 3’UTR of PINX1 mRNA; however, it is unclear whether they affect the migration, invasion, and proliferation of prostate cancer cells. In this paper, PCR and Western blot were used to detect the expression of miRNA-501-5p and PINX1 in prostate cancer cells PC3, LNCaP, and DU145, and normal prostate epithelial cells RWPE-1. Compared to the normal prostate epithelial cells, miRNA-501-5p expression in prostate cancer cells was increased, and the expression of PINX1 was decreased. The methyl thiazolyl tetrazolium assay was used to detect the migration, proliferation, and invasion of prostate cancer DU145 cells. It was found that suppressing the expression of miRNA-501-5p or overexpressing PINX1 could inhibit the proliferation and other biological behaviors of DU145 cells; at the same time, the level of Cyclin D1, MMP-2, and MMP-14 protein was decreased, and the protein level of P21 was increased. Moreover, inhibition of PINX1 expression could partially reverse miRNA-501-5p’s inhibitory effect on the migration, invasion, and proliferation of prostate cancer cells. Therefore, miRNA-501-5p targeted PINX1 for down-regulation to promote prostate cancer cell migration, invasion, and proliferation.

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