scholarly journals tRNALys-Derived Fragment Alleviates Cisplatin-Induced Apoptosis in Prostate Cancer Cells

Pharmaceutics ◽  
2021 ◽  
Vol 13 (1) ◽  
pp. 55
Author(s):  
Changwon Yang ◽  
Minkyeong Lee ◽  
Gwonhwa Song ◽  
Whasun Lim
Keyword(s):  
Prostate Cancer ◽  
Cancer Cells ◽  
Suppressor Gene ◽  
Prostate Cancer Cells ◽  
Apoptotic Pathway ◽  
Normal Prostate ◽  
Prostate Cells ◽  
Du145 Cells ◽  
Induced Apoptosis ◽  
Related Proteins

Cisplatin is a standard treatment for prostate cancer, which is the third leading cause of cancer-related deaths among men globally. However, patients who have undergone cisplatin can rxperience relapse. tRNA-derived fragments (tRFs) are small non-coding RNAs generated via tRNA cleavage; their physiological activities are linked to the development of human diseases. Specific tRFs, including tRF-315 derived from tRNALys, are highly expressed in prostate cancer patients. However, whether tRF-315 regulates prostate cancer cell proliferation or apoptosis is unclear. Herein, we confirmed that tRF-315 expression was higher in prostate cancer cells (LNCaP, DU145, and PC3) than in normal prostate cells. tRF-315 prevented cisplatin-induced apoptosis and alleviated cisplatin-induced mitochondrial dysfunction in LNCaP and DU145 cells. Moreover, transfection of tRF-315 inhibitor increased the expression of apoptotic pathway-related proteins in LNCaP and DU145 cells. Furthermore, tRF-315 targeted the tumor suppressor gene GADD45A, thus regulating the cell cycle, which was altered by cisplatin in LNCaP and DU145 cells. Thus, tRF-315 protects prostate cancer cells from mitochondrion-dependent apoptosis induced by cisplatin treatment.

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.

AS1 expression in prostate cancer and its effects on proliferation and invasion of prostate cancer cells

2021 ◽  
pp. 1-9
Author(s):  
Yuxin Li ◽  
Xiaohong Zhuang ◽  
Li Zhuang ◽  
Hongjian Liu
Keyword(s):  
Prostate Cancer ◽  
Cell Proliferation ◽  
Cancer Cells ◽  
Related Protein ◽  
Prostate Cancer Cells ◽  
Blank Group ◽  
Normal Prostate ◽  
Cell Cycles ◽  
Prostate Cells ◽  
Proliferation And Invasion

This paper aimed at investigating AS1 expression in prostate cancer (PCa) and its effects on the proliferation and invasion of prostate cancer cells (PCCs). The prostate tissues and the matched adjacent normal prostate tissues excised and preserved during radical prostatectomy in our hospital were collected. The LncRNA NCK1-AS1 expression was detected. PCa patients were followed up for three years to analyze their prognosis. The correlation of LncRNA NCK1-AS1 expression with clinicopathological features was analyzed. Human normal prostate cells and human PCCs were selected, in which LncRNA NCK1-AS1 expression was tested to screen and then transfect the cells. Cell proliferation, invasion and migration were detected. Cell cycles and apoptosis were analyzed. Compared with the adjacent normal tissues, LncRNA NCK1-AS1 was highly expressed in the prostate cancer tissues. Its expression was remarkably different in those with different stages of TNM and with lymphatic metastasis or not. The prognosis of patients with high LncRNA NCK1-AS1 expression was remarkably poorer than that of those with low expression. Compared with the human normal prostate cells, LncRNA NCK1-AS1 expression in the human PCCs remarkably rose, with the greatest difference in 22Rv1 cells. Compared with the Blank group, cell proliferation and the number of plate cloned cells remarkably reduced in the sh-NCK1-AS1 group. Additionally, in this group, the number of invasive and migratory cells remarkably reduced; the expression of invasion-related protein E-cadherin remarkably rose but that of MMP-2 remarkably reduced; cell cycles were arrested and the expression of cycle-related proteins (CDK4, CDK6, cyclin D1) remarkably reduced; the apoptotic rate and the expression of apoptosis-related protein Bax remarkably rose. LncRNA NCK1-AS1 is highly expressed in PCa, so its down-regulation can inhibit PCCs from proliferating and reduce the number of invasive cells.

scholarly journals Calcitriol-Induced Apoptosis in LNCaP Cells Is Blocked By Overexpression of Bcl-21

Endocrinology ◽  
2000 ◽  
Vol 141 (1) ◽  
pp. 10-17 ◽  
Author(s):  
Sarah E. Blutt ◽  
Timothy J. McDonnell ◽  
Tara C. Polek ◽  
Nancy L. Weigel
Keyword(s):  
Prostate Cancer ◽  
Cell Cycle ◽  
Vitamin D ◽  
Cancer Cells ◽  
Mineral Metabolism ◽  
Lncap Cells ◽  
Prostate Cancer Cells ◽  
Apoptotic Pathway ◽  
Induced Apoptosis

Abstract While the role of vitamin D in bone and mineral metabolism has been investigated extensively, the role of the vitamin D receptor in other tissues is less well understood. 1,25-dihydroxyvitamin D3 (calcitriol) can act as a differentiating agent in normal tissues and can inhibit the growth of many cancer cell lines including LNCaP prostate cancer cells. We have shown previously that calcitriol causes LNCaP cell accumulation in the G0/G1 phase of the cell cycle. In this study, we demonstrate that calcitriol also induces apoptosis of LNCaP cells. The calcitriol-induced apoptosis is accompanied by a down-regulation of Bcl-2 and Bcl-XL proteins, both of which protect cells from undergoing apoptosis. Other proteins important in apoptotic control, Bax, Mcl-1, and Bcl-Xs, are unaffected by calcitriol treatment. We find that overexpression of Bcl-2 blocks calcitriol-induced apoptosis and reduces, but does not eliminate, calcitriol-induced growth inhibition. We conclude that both regulation of cell cycle and the apoptotic pathway are involved in calcitriol action in prostate cancer cells.

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 Increased distributional variance of mitochondrial DNA content associated with prostate cancer cells as compared with normal prostate cells

The Prostate ◽  
2008 ◽  
Vol 68 (4) ◽  
pp. 408-417 ◽  
Author(s):  
Takatsugu Mizumachi ◽  
Levan Muskhelishvili ◽  
Akihiro Naito ◽  
Jun Furusawa ◽  
Chun-Yang Fan ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Mitochondrial Dna ◽  
Cancer Cells ◽  
Dna Content ◽  
Prostate Cancer Cells ◽  
Normal Prostate ◽  
Prostate Cells ◽  
Mitochondrial Dna Content

scholarly journals Annexin-A7 protects normal prostate cells and induces distinct patterns of RB-associated cytotoxicity in androgen-sensitive and -resistant prostate cancer cells

2009 ◽  
Vol 125 (11) ◽  
pp. 2528-2539 ◽  
Author(s):  
Yelizaveta Torosyan ◽  
Olga Simakova ◽  
Shanmugam Naga ◽  
Katerina Mezhevaya ◽  
Ximena Leighton ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cancer Cells ◽  
Prostate Cancer Cells ◽  
Normal Prostate ◽  
Prostate Cells ◽  
Annexin A7

scholarly journals hPEBP4 Resists TRAIL-induced Apoptosis of Human Prostate Cancer Cells by Activating Akt and Deactivating ERK1/2 Pathways

2006 ◽  
Vol 282 (7) ◽  
pp. 4943-4950 ◽  
Author(s):  
Hongzhe Li ◽  
Xiaojian Wang ◽  
Nan Li ◽  
Jianming Qiu ◽  
Yuanyuan Zhang ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cancer Treatment ◽  
Cancer Cells ◽  
Potential Candidate ◽  
Lncap Cells ◽  
Prostate Cancer Cells ◽  
Efficient Treatment ◽  
Akt Activation ◽  
Du145 Cells ◽  
Induced Apoptosis

The treatment options available for prostate cancer are limited because of its resistance to therapeutic agents. Thus, a better understanding of the underlying mechanisms of the resistance of prostate cancer will facilitate the discovery of more efficient treatment protocols. Human phosphatidylethanolamine-binding protein 4 (hPEBP4) is recently identified by us as an anti-apoptotic molecule and a potential candidate target for breast cancer treatment. Here we found the expression levels of hPEBP4 were positively correlated with the severity of clinical prostate cancer. Furthermore, hPEBP4 was not expressed in TRAIL-sensitive DU145 prostate cancer cells, but was highly expressed in TRAIL-resistant LNCaP cells, which show highly activated Akt. Interestingly, hPEBP4 overexpression in TRAIL-sensitive DU145 cells promoted Akt activation but inhibited ERK1/2 activation. The hPEBP4-overexpressing DU145 cells became resistant to TRAIL-induced apoptosis consequently, which could be reversed by PI3K inhibitors. In contrast, silencing of hPEBP4 in TRAIL-resistant LNCaP cells inhibited Akt activation but increased ERK1/2 activation, resulting in their sensitivity to TRAIL-induced apoptosis that was restored by the MEK1 inhibitor. Therefore, hPEBP4 expression in prostate cancer can activate Akt and deactivate ERK1/2 signaling, leading to TRAIL resistance. We also demonstrated that hPEBP4-mediated resistance to TRAIL-induced apoptosis occurred downstream of caspase-8 and at the level of BID cleavage via the regulation of Akt and ERK pathways, and that hPEBP4-regulated ERK deactivation was upstream of Akt activation in prostate cancer cells. Considering that hPEBP4 confers cellular resistance to TRAIL-induced apoptosis and is abundantly expressed in poorly differentiated prostate cancer, silencing of hPEBP4 suggests a promising approach for prostate cancer treatment.

KLK31P is a novel androgen regulated and transcribed pseudogene of kallikreins that is expressed at lower levels in prostate cancer cells than in normal prostate cells

The Prostate ◽  
2006 ◽  
Vol 66 (9) ◽  
pp. 936-944 ◽  
Author(s):  
Wei Lu ◽  
Daixing Zhou ◽  
Gustavo Glusman ◽  
Angelita G. Utleg ◽  
James T. White ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cancer Cells ◽  
Prostate Cancer Cells ◽  
Normal Prostate ◽  
Prostate Cells

Evaluation of a nonlinear Hertzian-based model reveals prostate cancer cells respond differently to force than normal prostate cells

2012 ◽  
Vol 76 (1) ◽  
pp. 36-41 ◽  
Author(s):  
M.F. Murphy ◽  
F. Lilley ◽  
M.J. Lalor ◽  
S.R. Crosby ◽  
G. Madden ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cancer Cells ◽  
Prostate Cancer Cells ◽  
Normal Prostate ◽  
Prostate Cells

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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