ErbB kinases and NDF signaling in human prostate cancer cells

Grasso, Adam W.; Wen, Duanzhi; Miller, Clinton; Rhim, Johng S.; Pretlow, Thomas G.; Kung, Hsing Jien

doi:10.1038/sj.onc.1201447

Cited by 133 publications

(133 citation statements)

References 53 publications

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“…The EGFR/PI-3K pathway, 59 PI-3/ Akt pathway, 60,61 EGFR/Ras/MAPK pathway, 62 and the NF-kB pathway 63 play key roles in cellular proliferation and cell survival. These pathways are hyperactivated in a number of human tumors including the prostate cancer.…”

Section: (3) Antagonistic Signaling Pathways Of Tgf-b Mediated Apoptomentioning

confidence: 99%

“…These pathways are hyperactivated in a number of human tumors including the prostate cancer. 62 In BPH, increased levels of EGFR and the related HER2/ neu signaling pathways have also been associated with loss of growth control. 64 -66 Downstream elements of the EGFR pathway have inhibitory effects on the Smad elements of the TGF-b signaling, potentially pathway via a Ras mediated mechanism 67 and the transcriptional co-repressor, TGIF.…”

Section: (3) Antagonistic Signaling Pathways Of Tgf-b Mediated Apoptomentioning

confidence: 99%

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Induction of prostate apoptosis by α1-adrenoceptor antagonists: mechanistic significance of the quinazoline component

Anglin

Glassman

Kyprianou

2002

Prostate Cancer Prostatic Dis

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a 1 -Adrenoceptor antagonists, have been documented to induce apoptosis and reduce prostate tumor vascularity in benign and malignant prostate cells. The quinazoline based a 1 -antagonists, doxazosin and terazosin but not tamsulosin (a sulphonamide derivative) suppress prostate growth without affecting cell proliferation. These quinazoline-mediated apoptotic effects occur via an a 1 -adrenoceptor independent mechanism potentially involving activation of the TGF-b signal transduction pathway. This review discusses the current knowledge of the action of quinazoline-derived a 1 -adrenoceptor antagonists in the benign and malignant prostate and their potential therapeutic use in the treatment of benign prostatic hyperplasia (BPH) and prostate cancer. Finally, a molecular pathway is proposed for their observed apoptotic function against prostate cells. Increased understanding of the action of these established and clinically accepted agents would provide a basis for the design of safe, effective therapeutic regimens in the treatment of prostatic diseases.

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Section: (3) Antagonistic Signaling Pathways Of Tgf-b Mediated Apoptomentioning

confidence: 99%

Section: (3) Antagonistic Signaling Pathways Of Tgf-b Mediated Apoptomentioning

confidence: 99%

Induction of prostate apoptosis by α1-adrenoceptor antagonists: mechanistic significance of the quinazoline component

Anglin

Glassman

Kyprianou

2002

Prostate Cancer Prostatic Dis

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“…HRG mRNA could be detected in these cell lines only by RT -PCR in one study (Lyne et al, 1997), but was not detected in another (Grasso et al, 1997a). HRG inhibits growth and induces differentiation of AR positive, ErbB1 -3 positive LNCaP cells, but has little effect on proliferation of ErbB1 -3 positive, AR negative DU 145 and PC-3 cells (Grasso et al, 1997b;Lyne et al, 1997). In addition, HRG induces the expression of the tumour suppressor p53 and the CDK inhibitor p21 in LNCaP cells (Bacus et al, 1996).…”

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confidence: 99%

“…By contrast, the ErbB3/4 ligand HRG is highly expressed in basal, luminal and stromal cells of the normal prostate, but not in prostate tumours (Lyne et al, 1997). Further, HRG protein is not detected in the prostate cancer cell lines LNCaP, DU-145 or PC-3 (Grasso et al, 1997a;Lyne et al, 1997). HRG mRNA could be detected in these cell lines only by RT -PCR in one study (Lyne et al, 1997), but was not detected in another (Grasso et al, 1997a).…”

mentioning

confidence: 99%

“…Further, HRG protein is not detected in the prostate cancer cell lines LNCaP, DU-145 or PC-3 (Grasso et al, 1997a;Lyne et al, 1997). HRG mRNA could be detected in these cell lines only by RT -PCR in one study (Lyne et al, 1997), but was not detected in another (Grasso et al, 1997a). HRG inhibits growth and induces differentiation of AR positive, ErbB1 -3 positive LNCaP cells, but has little effect on proliferation of ErbB1 -3 positive, AR negative DU 145 and PC-3 cells (Grasso et al, 1997b;Lyne et al, 1997).…”

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confidence: 99%

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Specificity and heregulin regulation of Ebp1 (ErbB3 binding protein 1) mediated repression of androgen receptor signalling

Zhang

Hamburger

2004

Br J Cancer

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Although ErbB receptors have been implicated in the progression of prostate cancer, little is known about proteins that may mediate their interactions with the androgen receptor (AR). Ebp1, a protein cloned via its association with the ErbB3 receptor, binds the AR and inhibits androgen-regulated transactivation of wild-type AR in COS cells. As the complement of coregulators in different cells are important for AR activity, we determined the effect of Ebp1 on AR function in prostate cancer cell lines. In addition, we examined the regulation of Ebp1 function by the ErbB3/4 ligand heregulin (HRG). In this study, we demonstrate, using several natural AR-regulated promoters, that Ebp1 repressed transcriptional activation of wild-type AR in prostate cancer cell lines. Downregulation of Ebp1 expression in LNCaP cells using siRNA resulted in activation of AR in the absence of androgen. Ebp1 associated with ErbB3 in LNCaP cells in the absence of HRG, but HRG induced the dissociation of Ebp1 from ErbB3. In contrast, HRG treatment enhanced both the association of Ebp1 with AR and also the ability of Ebp1 to repress AR transactivation. These studies suggest that Ebp1 is an AR corepressor whose biological activity can be regulated by the ErbB3 ligand, HRG.

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Overexpression of the EphA2 tyrosine kinase in prostate cancer

et al. 1999

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BACKGROUND Molecules that are highly expressed by human prostate cancers may serve as therapeutically relevant targets or tumor markers. Tyrosine kinases are frequently overexpressed in metastatic tumor cells and this prompted us to screen for tyrosine kinases that are overexpressed in prostate cancer cells. METHODS Expression levels of the EphA2 receptor tyrosine kinase were determined by Western blot analysis in canine and human prostate cancer cell lines and in immortalized and transformed variants of 267B1 prostatic epithelial cells. EphA2 levels in benign human prostate and prostate cancers were also determined in formalin‐fixed, paraffin‐embedded tissues using immunohistochemical staining. RESULTS Metastatic prostate cancer cells overexpressed EphA2 by 10‐100 fold as compared with non‐invasive prostatic epithelial cells. EphA2 immunoreactivity in vivo was also significantly greater in human prostate cancers as compared with benign prostate epithelium. CONCLUSIONS The EphA2 receptor tyrosine kinase is differentially expressed in human and canine prostate cancer cell lines and overexpressed in human prostate cancers as compared with benign prostate tissues. Metastasis‐derived canine prostate carcinoma cell lines overexpress EphA2 and may provide pre‐clinical models to further evaluate the role of EphA2 in prostate carcinogenesis. Further investigations are needed to determine the utility of EphA2 as a tumor marker and a novel target in human prostate cancer. Prostate 41:275–280, 1999. © 1999 Wiley‐Liss, Inc.

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ErbB kinases and NDF signaling in human prostate cancer cells

Cited by 133 publications

References 53 publications

Induction of prostate apoptosis by α1-adrenoceptor antagonists: mechanistic significance of the quinazoline component

Induction of prostate apoptosis by α1-adrenoceptor antagonists: mechanistic significance of the quinazoline component

Specificity and heregulin regulation of Ebp1 (ErbB3 binding protein 1) mediated repression of androgen receptor signalling

Overexpression of the EphA2 tyrosine kinase in prostate cancer

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