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.

scholarly journals DNMT1 and DNMT3B regulate tumorigenicity of human prostate cancer cells by controlling RAD9 expression through targeted methylation

2020 ◽  
Author(s):  
Aiping Zhu ◽  
Kevin M Hopkins ◽  
Richard A Friedman ◽  
Joshua D Bernstock ◽  
Constantinos G Broustas ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cancer Cells ◽  
Ectopic Expression ◽  
Dna Methyltransferases ◽  
Prostate Cancer Cells ◽  
Normal Prostate ◽  
Prostate Tumorigenesis ◽  
Du145 Cells ◽  
Cpg Hypermethylation ◽  
High Level

Abstract Prostate cancer is the second most common type of cancer and the second leading cause of cancer death in American men. RAD9 stabilizes the genome, but prostate cancer cells and tumors often have high quantities of the protein. Reduction of RAD9 level within prostate cancer cells decreases tumorigenicity of nude mouse xenographs and metastasis phenotypes in culture, indicating that RAD9 overproduction is essential for the disease. In prostate cancer DU145 cells, CpG hypermethylation in a transcription suppressor site of RAD9 intron 2 causes high-level gene expression. Herein, we demonstrate that DNA methyltransferases DNMT1 and DNMT3B are highly abundant in prostate cancer cells DU145, CWR22, LNCaP and PC-3; yet, these DNMTs bind primarily to the transcription suppressor in DU145, the only cells where methylation is critical for RAD9 regulation. For DU145 cells, DNMT1 or DNMT3B shRNA reduced RAD9 level and tumorigenicity, and RAD9 ectopic expression restored this latter activity in the DNMT knockdown cells. High levels of RAD9, DNMT1, DNMT3B and RAD9 transcription suppressor hypermethylation were significantly correlated in prostate tumors, and not in normal prostate tissues. Based on these results, we propose a novel model where RAD9 is regulated epigenetically by DNMT1 and DNMT3B, via targeted hypermethylation, and that consequent RAD9 overproduction promotes prostate tumorigenesis.

scholarly journals Effects of Sulforaphane and 3,3′-Diindolylmethane on Genome-Wide Promoter Methylation in Normal Prostate Epithelial Cells and Prostate Cancer Cells

PLoS ONE ◽  
2014 ◽  
Vol 9 (1) ◽  
pp. e86787 ◽  
Author(s):  
Carmen P. Wong ◽  
Anna Hsu ◽  
Alex Buchanan ◽  
Zoraya Palomera-Sanchez ◽  
Laura M. Beaver ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Epithelial Cells ◽  
Cancer Cells ◽  
Promoter Methylation ◽  
Prostate Cancer Cells ◽  
Normal Prostate ◽  
Prostate Epithelial Cells ◽  
Genome Wide

scholarly journals Cytostatic Action of Novel Histone Deacetylase Inhibitors in Androgen Receptor-Null Prostate Cancer Cells

2021 ◽  
Vol 14 (2) ◽  
pp. 103
Author(s):  
Zohaib Rana ◽  
Joel D. A. Tyndall ◽  
Muhammad Hanif ◽  
Christian G. Hartinger ◽  
Rhonda J. Rosengren
Keyword(s):  
Prostate Cancer ◽  
Androgen Receptor ◽  
Cancer Cells ◽  
Hdac Inhibitors ◽  
G1 Arrest ◽  
Prostate Cancer Cells ◽  
Prostate Tumors ◽  
Normal Prostate ◽  
Pc3 Cells ◽  
Du145 Cells

Androgen receptor (AR)-null prostate tumors have been observed in 11–24% of patients. Histone deacetylases (HDACs) are overexpressed in prostate tumors. Therefore, HDAC inhibitors (Jazz90 and Jazz167) were examined in AR-null prostate cancer cell lines (PC3 and DU145). Both Jazz90 and Jazz167 inhibited the growth of PC3 and DU145 cells. Jazz90 and Jazz167 were more active in PC3 cells and DU145 cells in comparison to normal prostate cells (PNT1A) and showed a 2.45- and 1.30-fold selectivity and higher cytotoxicity toward DU145 cells, respectively. Jazz90 and Jazz167 reduced HDAC activity by ~60% at 50 nM in PC3 lysates. At 4 μM, Jazz90 and Jazz167 increased acetylation in PC3 cells by 6- to 8-fold. Flow cytometry studies on the cell phase distribution demonstrated that Jazz90 causes a G0/G1 arrest in AR-null cells, whereas Jazz167 leads to a G0/G1 arrest in DU145 cells. However, apoptosis only occurred at a maximum of 7% of the total cell population following compound treatments in PC3 and DU145 cells. There was a reduction in cyclin D1 and no significant changes in bcl-2 in DU145 and PC3 cells. Overall, the results showed that Jazz90 and Jazz167 function as cytostatic HDAC inhibitors in AR-null prostate cancer cells.

scholarly journals eIF5B regulates the expression of PD-L1 in prostate cancer cells by interacting with Wig1

BMC Cancer ◽  
2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Qi Li ◽  
Mulun Xiao ◽  
Yibo Shi ◽  
Jinhao Hu ◽  
Tianxiang Bi ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cancer Cells ◽  
Tumor Cells ◽  
Translation Initiation ◽  
Genetic Alterations ◽  
Cell Counting ◽  
Migration And Invasion ◽  
Cell Group ◽  
Prostate Cancer Cells ◽  
Normal Prostate

Abstract Background Eukaryotic translation initiation factors (eIFs) are the key factors to synthesize translation initiation complexes during the synthesis of eukaryotic proteins. Besides, eIFs are especially important in regulating the immune function of tumor cells. However, the effect mechanism of eIFs in prostate cancer remains to be studied, which is precisely the purpose of this study. Methods In this study, three groups of prostate cancer cells were investigated. One group had its eIF5B gene knocked down; another group had its Programmed death 1 (PD-L1) overexpressed; the final group had its Wild-type p53-induced gene 1 (Wig1) overexpressed. Genetic alterations of the cancer cells were performed by plasmid transfection. The expression of PD-L1 mRNA was detected by quantitative real-time PCR (qRT-PCR), and the expressions of PD-L1 and eIF5B proteins were observed by western blot assays. Cell Counting Kit-8 (CCK-8), flow cytometry, Transwell and Transwell martrigel were used to investigated cell proliferation, apoptosis, migration and invasion, respectively. The effect of peripheral blood mononuclear cells (PBMCs) on tumor cells was observed, and the interaction between eIF5B and Wig1 was revealed by co-immunoprecipitation (CoIP) assay. Finally, the effects of interference with eIF5B expression on the growth, morphology, and immunity of the tumor, as well as PD-L1 expression in the tumor, were verified by tumor xenograft assays in vivo. Results Compared with normal prostate epithelial cells, prostate cancer cells revealed higher expressions of eIF5B and PD-L1 interference with eIF-5B expression can inhibit the proliferation, migration, invasion and PD-L1 expression of prostate cancer cells. Meanwhile, the cancer cell group with interference with eIF5B expression also demonstrated greater, apoptosis and higher vulnerability to PBMCs. CoIP assays showed that Wig1 could bind to eIF5B in prostate cancer cells, and its overexpression can inhibit the proliferation, migration, invasion and PD-L1 expression of cancer cells while promoting apoptosis. Moreover, interference with eIF5B expression can inhibit tumor growth, destroy tumor morphology, and suppress the proliferation of tumor cells. Conclusion eIF5B can promote the expression of PD-L1 by interacting with Wig1. Besides, interference with eIF5B expression can inhibit the proliferation, migration, invasion and immunosuppressive response of prostate cancer cells. This study proposes a new target, eIF5B, for immunotherapy of prostate cancer.

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
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