DJ-1 and androgen receptor immunohistochemical expression in prostatic carcinoma: A possible role in carcinogenesis

Osman, Wesam M.; Atti, Rasha M. Abd El; Gabal, Hoda H. Abou

doi:10.1016/j.jnci.2013.08.001

Cited by 10 publications

(15 citation statements)

References 34 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…19) Increasing evidences pointed that AR was a critical mediator for anti-prostate cancer. [20][21][22] In view of this, researchers tended to explore agents to antagonize AR as improved therapeutic methods for prostatic cancer. A natural prenylflavonoid, also known as icaritin (ICT), inhibited AR-regulated genes in AR-positive prostate cancer cells via AR-depended pathways.…”

Section: Discussionmentioning

confidence: 99%

<i>Artesunate</i> Suppresses the Growth of Prostatic Cancer Cells through Inhibiting Androgen Receptor

Wang¹,

Wang²,

et al. 2017

Biological & Pharmaceutical Bulletin

View full text Add to dashboard Cite

Prostatic cancer (PCa) is a leading cause of cancer related death in males and is often regarded as a kind of androgen-sensitive cancer. Artesunate (ART), a semi-synthetic derivative of the Chinese herb Artemisia annua, is such an anti-cancer agent. However, the effects and mechanism of ART on PCa cells remains unclear. The study aims to elaborate the mechanism of the involvement of androgen receptor (AR) in antiprostatic cancer (PCa) of artesunate (ART). PCa cells 22rvl were used in vivo and in vitro, and the viability and apoptosis were conducted using 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2H-tetrazolium bromide (MTT) and terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick-end labeling (TUNEL) assay, respectively. Ectopic expressions of AR and DNA methyltransferase (DNMT) were detected in cells in overexpression or interference of AR or DNMT3b. ART dose-dependently suppressed tumor growth, inhibited cell viability, enhanced apoptosis, decreased AR expression, and increased the expression and the catalytic activity of DNMT3b in 22rv1 cells either in transplanted mice or in vitro. Furthermore, AR downregulated DNMT3b expression, and overexpression of AR or interference of DNMT3b could reverse ART-induced cytotoxicity and apoptosis in 22rvl cells, whereas overexpression of DNMT3b could not change the effect profiles of ART on the cells. The results indicated that ART suppressed tumor growth of prostatic cancer cells through AR-DNMT3b pathway, underlying ART will allow for the utilization of this Chinese therapeutic agent for the potential treatment of prostate cancer.Key words artesunate; prostatic cancer; androgen receptor; DNA methyltransferase; apoptosis Prostatic cancer (PCa) is the most common cause of cancerrelated death in males. Morbidity and mortality of PCa underscore the need for novel treatment options. Although improved therapies have been recently developed to treat and prevent PCa, prostate cancer still remains refractory disease. Lately, herbs and phytochemicals 1) have been attractive as therapeutic agents for tumorigenesis suppression. Understanding how the production of these Chinese herbs is regulated during cancer progression would help develop new cancer therapeutic strategy.Artesunate (ART) is a semi-synthetic derivative of artemisinin, the active principle of the Chinese herb Artemisia annua. ART has been revealed remarkable activity against otherwise multidrug-resistant Plasmodium falciparum and P. vivax malaria. With the recognition of ART, it has now been analyzed for its anti-cancer activity in various tissues-specificity. For example, Tran et al. found that enhancement of ART activity could effectively induce the apoptosis of breast cancer cells. 2)Moreover, ART was proved to be as a novel therapeutic agent for metastatic renal cell carcinoma due to its attenuation action on tumor growth, metastasis.3) Recently, Michaelsen et al. clinically treated PCa patients with long-term Artemisia annua capsules via oral administration combined with shortterm ART inj...

show abstract

Section: Discussionmentioning

confidence: 99%

<i>Artesunate</i> Suppresses the Growth of Prostatic Cancer Cells through Inhibiting Androgen Receptor

Wang¹,

Wang²,

et al. 2017

Biological & Pharmaceutical Bulletin

View full text Add to dashboard Cite

show abstract

“…It is well accepted that DJ‐1 plays a critical role in the development of PCa mediated by AR signaling (Tillman et al, ; Osman et al, ), yet the detailed mechanism remains vague, which leaves a very interesting scientific question for the investigation. The effect of DJ‐1 on autophagic activity has been verified in other types of cell (Ren et al, ) but never in PCa.…”

Section: Discussionmentioning

confidence: 99%

“…Moreover, DJ‐1 binds AR to stimulate its transcriptional activity in androgen‐treated PCa cells, which contributes to the function of androgen and progression of PCa (Tillman et al, ). More important, the value of DJ‐1 immunohistochemical expression in the diagnosis of PCa has been proved (Osman et al, ). Not only is there a significant correlation of immunohistochemical scores between DJ‐1 and AR, but DJ‐1 is more specific than AR (Osman et al, ).…”

Section: Introductionmentioning

confidence: 99%

“…More important, the value of DJ‐1 immunohistochemical expression in the diagnosis of PCa has been proved (Osman et al, ). Not only is there a significant correlation of immunohistochemical scores between DJ‐1 and AR, but DJ‐1 is more specific than AR (Osman et al, ). It was suggested that DJ‐1 provides an ideal complement to AR in the diagnosis and treatment of PCa.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

DJ‐1 inhibits autophagy activity of prostate cancer cells by repressing JNK–Bcl2–Beclin1 signaling

Qin¹,

Lu²,

Ke³

et al. 2020

Cell Biology International

View full text Add to dashboard Cite

The regulation of DJ‐1 on AR signaling plays an important role in the pathogenesis of prostate cancer (PCa). DJ‐1 could alter autophagy and regulate Beclin1‐involved autophagy response through JNK‐dependent pathway. JNK is known to mediate autophagy through Bcl2–Beclin1 complex. Therefore, this study aimed to investigate the significance of autophagy in DJ‐1‐modulated PCa cells. The current studies showed that DJ‐1 overexpression in LNCaP decreased LC3 transformation and autophagosome formation. However, DJ‐1 knockdown exerted the opposite effect. Moreover, DJ‐1 silencing inhibited survival and promoted death in LNCaP, which was recovered by autophagy inhibition with 3‐MA. In addition, DJ‐1 overexpression inhibited the phosphorylation of JNK and Bcl2, and the dissociation of Beclin1 and Bcl2; while the effect of silencing DJ‐1 was completely opposite. More important, JNK activated by anisimycin inhibited the proliferation and promoted death of DJ‐1‐overexpressed LNCaP while increasing LC3 transformation and LC3‐puncta formation, but these results were reversed by the decrease of Beclin1 (by spautin‐1). In contrast, when DJ‐1 was silenced, the death of LNCaP, LC3 transformation, and LC3‐puncta formation were inhibited by JNK inhibitor SP600125, which promoted cell proliferation. However, Bcl2 inhibition (by ABT737) reversed all the effects of SP600125. Our results suggested that DJ‐1 in PCa cells could promote the growth of PCa through autophagy inhibition, and JNK–Bcl2–Beclin1 signaling played an important role in it. The study provided new insights into the role of DJ‐1 in the development of PCa.

show abstract

“…63) DJ-1 is translocated from the cytoplasm to nucleus upon addition of a mitogen to the culture medium 26) and is translocated to mitochondria after oxidative stress. 64) Increased levels of DJ-1 expression have been observed in various cancer cells and tissues, including breast, 51,52) prostate, 65,66) lung, 67,68) and endometrial, 69,70) thyroid, 71,72) pancreas, [73][74][75][76] esophageal, 77) ovary, 78,79) cervical, 80) liver, 81) gastric, 82 57,90) and leukemia. 91,92) Secretion of DJ-1 into the serum or nipple fluid has been found in patients with breast cancer.…”

Section: Tumor Suppressor Mm-1 and Neurodegenerationmentioning

confidence: 99%

Common Mechanisms of Onset of Cancer and Neurodegenerative Diseases

Ariga

2015

Biological & Pharmaceutical Bulletin

View full text Add to dashboard Cite

Onset of cancer and neurodegenerative disease occurs by abnormal cell growth and neuronal cell death, respectively, and the number of patients with both diseases has been increasing in parallel with an increase in mean lifetime, especially in developed countries. Although both diseases are sporadic, about 10% of the diseases are genetically inherited, and analyses of such familial forms of gene products have contributed to an understanding of the molecular mechanisms underlying the onset and pathogenesis of these diseases. I have been working on c-myc, a protooncogene, for a long time and identified various c-Myc-binding proteins that play roles in c-Myc-derived tumorigenesis. Among these proteins, some proteins have been found to be also responsible for the onset of neurodegenerative diseases, including Parkinson's disease, retinitis pigmentosa and cerebellar atrophy. In this review, I summarize our findings indicating the common mechanisms of onset between cancer and neurodegenerative diseases, with a focus on genes such as DJ-1 and Myc-Modulator 1 (MM-1) and signaling pathways that contribute to the onset and pathogenesis of cancer and neurodegenerative diseases.

show abstract

DJ-1 and androgen receptor immunohistochemical expression in prostatic carcinoma: A possible role in carcinogenesis

Cited by 10 publications

References 34 publications

<i>Artesunate</i> Suppresses the Growth of Prostatic Cancer Cells through Inhibiting Androgen Receptor

<i>Artesunate</i> Suppresses the Growth of Prostatic Cancer Cells through Inhibiting Androgen Receptor

DJ‐1 inhibits autophagy activity of prostate cancer cells by repressing JNK–Bcl2–Beclin1 signaling

Common Mechanisms of Onset of Cancer and Neurodegenerative Diseases

Contact Info

Product

Resources

About