NF-κB and TNF-α stimulate androgen receptor expression in Sertoli cells

Delfino, Frank J.; Boustead, Jared N.; Fix, Charity; Walker, William H.

doi:10.1016/s0303-7207(03)00005-4

Cited by 82 publications

(71 citation statements)

References 59 publications

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“…6C). Next, we determined the effect of guggulsterone treatment on promoter activity of androgen receptor by luciferase reporter assay using pARLUC plasmid (48), and the results are summarized in Fig. 6D.…”

Section: Resultsmentioning

confidence: 99%

“…These results suggest that the guggulsterone-mediated decline in protein level of androgen receptor is probably the result of repression of the androgen receptor promoter. Previous studies have shown that androgen receptor promoter activity is stimulated by overexpression of NF-nB subunits in Sertoli cells (48). Because guggulsterone treatment inhibits NF-nB activation (15), it seems reasonable to postulate that guggulsteronemediated inhibition of androgen receptor promoter in LNCaP cells may be caused by inhibition of NF-nB.…”

Section: Discussionmentioning

confidence: 97%

See 1 more Smart Citation

Guggulsterone-Induced Apoptosis in Human Prostate Cancer Cells Is Caused by Reactive Oxygen Intermediate–Dependent Activation of c-Jun NH2-Terminal Kinase

et al. 2007

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Guggulsterone, a constituent of Indian Ayurvedic medicinal plant Commiphora mukul, causes apoptosis in cancer cells but the sequence of events leading to cell death is poorly understood. We now show that guggulsterone-induced cell death in human prostate cancer cells is caused by reactive oxygen intermediate (ROI)-dependent activation of c-Jun NH 2 -terminal kinase (JNK). Exposure of PC-3 and LNCaP cells to apoptosis inducing concentrations of guggulsterone resulted in activation of JNK and p38 mitogen-activated protein kinase (p38 MAPK) in both cell lines and activation of extracellular signal-regulated kinase 1/2 (ERK1/2) in LNCaP cells. The guggulsterone-induced apoptosis in PC-3/LNCaP cells was partially but statistically significantly attenuated by pharmacologic inhibition (SP600125) as well as genetic suppression of JNK activation. On the other hand, pharmacologic inhibition of p38 MAPK activation in PC-3 or LNCaP cells (SB202190) and ERK1/2 activation in LNCaP cells (PD98059) did not protect against guggulsterone-induced cell death. The guggulsterone treatment caused generation of ROI in prostate cancer cells but not in a normal prostate epithelial cell line (PrEC), which was also resistant to guggulsteronemediated JNK activation. The guggulsterone-induced JNK activation as well as cell death in prostate cancer cells was significantly attenuated by overexpression of catalase and superoxide dismutase. In addition, guggulsterone treatment resulted in a decrease in protein level and promoter activity of androgen receptor in LNCaP cells. In conclusion, the present study reveals that the guggulsterone-induced cell death in human prostate cancer cells is regulated by ROI-dependent activation of JNK and guggulsterone inhibits promoter activity of androgen receptor. [Cancer Res 2007;67(15):7439-49]

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Section: Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 97%

Guggulsterone-Induced Apoptosis in Human Prostate Cancer Cells Is Caused by Reactive Oxygen Intermediate–Dependent Activation of c-Jun NH2-Terminal Kinase

et al. 2007

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“…These findings suggest that cytokines (e.g., TGF-␤2, TGF-␤3, TNF␣, IL-1␣) play a "commanding" role in regulating BTB dynamics and that they do not just regulate protein adhesion at the Sertoli-Sertoli cell interface via changes in the kinetics of endocytosis, recycling, and endosome-or ubiquitinmediated protein degradation (Yan et al, 2008b;Xia et al, 2009;Su et al, 2010b;Lie et al, 2011b) or proteinprotein interactions (Xiao et al, 2011). Instead, cytokines also work with polarity proteins, which are critical to regulate endocytic vesicle-mediated protein-trafficking events (Wong et al, 2010a), as well as actin dynamics (Sarkar et al, 2008;Lie et al, 2011b) and steroidmediated actions at the BTB (Delfino et al, 2003;Xiao et al, 2011). Herein, we will critically evaluate the central "commanding" role of cytokines on BTB regulation based on recent findings in the literature.…”

Section: Cytokinesmentioning

confidence: 99%

“…In short, TNF␣ is a multifunctional cytokine in the testis. For instance, it stimulates Sertoli cell androgen receptor expression, iron transport to germ cells, and lactate supply to postmeiotic germ cells; it regulates spermiation (Delfino et al, 2003;Siu et al, 2003a;Lysiak, 2004); and TNF␣ is also a potent inhibitor of Leydig cell steroidogenesis (Hong et al, 2004). In the testis, TFNR1 is mostly expressed in Leydig cells, lymphocytes, macrophages, Sertoli cells, and germ cells, whereas TNFR2 is detected in peritubular myoid and Sertoli cells (Pentikä inen et al, 2001;Suescun et al, 2003;Schell et al, 2008).…”

Section: Cheng and Mrukmentioning

confidence: 99%

The Blood-Testis Barrier and Its Implications for Male Contraception

2011

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“…NF-kB has been implicated in the repression of the AR gene promoter (Supakar et al, 1995;Nakajima et al, 1996). Paradoxically, in Sertoli cells, NF-kB elements in the AR promoter have been identified as being responsible for increased AR expression, representing an important (cell type-specific) regulatory mechanism required to maintain efficient spermatogenesis (Delfino et al, 2003). Much like the reciprocal cross-talk between ER and NF-kB in breast cancer, NF-kB activation blocks the proliferation of androgen-dependent prostate cancer cells, whereas the proliferation of cancer cells devoid of AR is not affected by NF-kB activation (Nakajima et al, 1996).…”

Section: Cross-talk Between Nf-jb and The Armentioning

confidence: 99%

Cross-talk between nuclear receptors and nuclear factor κB

2006

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A variety of studies have shown that some activated nuclear receptors (NRs), especially the glucorticoid receptor, the estrogen receptor and peroxisome proliferator-activated receptor, can inhibit the activity of the transcription factor nuclear factor jB (NF-jB), which plays a key role in the control of genes involved in inflammation, cell proliferation and apoptosis. This review describes the molecular mechanisms of cross-talk between NRs and NF-jB and the biological relevance of this crosstalk. The importance and mechanistic aspects of selective NR modulation are discussed. Also included are future research prospects, which will lead to a new era in the field of NR research with the aim of specifically inhibiting NF-jB-driven gene expression for anti-inflammatory, anti-tumor and immune-modulatory purposes.

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NF-κB and TNF-α stimulate androgen receptor expression in Sertoli cells

Cited by 82 publications

References 59 publications

Guggulsterone-Induced Apoptosis in Human Prostate Cancer Cells Is Caused by Reactive Oxygen Intermediate–Dependent Activation of c-Jun NH2-Terminal Kinase

Guggulsterone-Induced Apoptosis in Human Prostate Cancer Cells Is Caused by Reactive Oxygen Intermediate–Dependent Activation of c-Jun NH2-Terminal Kinase

The Blood-Testis Barrier and Its Implications for Male Contraception

Cross-talk between nuclear receptors and nuclear factor κB

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