Interleukin-8 signaling promotes androgen-independent proliferation of prostate cancer cells via induction of androgen receptor expression and activation

Seaton, Angela; Scullin, Paula; Maxwell, Pamela; Wilson, Catherine; Pettigrew, Johanna; Gallagher, R; O’Sullivan, Joe M.; Johnston, Patrick G.; Waugh, David J.

doi:10.1093/carcin/bgn109

Cited by 125 publications

(107 citation statements)

References 32 publications

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“…Indeed, the stable transfection of CXCL8 cDNA in AR-positive PCa cells reduces their dependence to androgens and reduces the growth inhibition observed in the presence of anti-androgens as bicalutamide, through CXCR1 (Araki et al 2007). On the other hand, Seaton et al (2008) reported that CXCL8 could enhance the proliferation of cancer cells, but this could not be observed in the presence of bicalutamide. Another difference with the study from Araki was that CXCL8 action occurred through CXCR2 (Seaton et al 2008).…”

Section: Do Chemokines Modulate Hormone Escape?mentioning

confidence: 92%

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Emerging roles of chemokines in prostate cancer

Vindrieux¹,

Escobar²,

Lazennec³

2009

Endocrine-Related Cancer

119

107

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Prostate cancer (PCa) represents the second leading cause of death among all cancer types in men in Europe and North America. Among the factors suspected to control PCa, incidence and progression, chemokines, and their receptors are now intensively studied. Chemokines are produced by tumor cells and also by the stromal microenvironment, both in the primary tumor site and in distant metastatic locations. The wide and differential distribution of chemokines and their receptors account for the pleiotropic actions of chemokines in PCa, including the modulation of growth, angiogenesis, invasion, metastasis, and hormone escape. This review will focus on the roles and the mechanisms of action and regulation of chemokines in the different steps of PCa development and will discuss the novel strategies that are currently envisioned to target chemokines in PCa.

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Section: Do Chemokines Modulate Hormone Escape?mentioning

confidence: 92%

“…CXCL8 enhances in vitro growth, motility, and invasion, as well as MMP-9 and VEGF production (Reiland et al 1999, Inoue et al 2000, Seaton et al 2008. In vivo, the stable transfection of CXCL8 in PCa cells stimulates tumor growth, probably through an increased angiogenesis (Inoue et al 2000, Lee et al 2004, Araki et al 2007).…”

Section: Chemokinesmentioning

confidence: 99%

Emerging roles of chemokines in prostate cancer

Vindrieux¹,

Escobar²,

Lazennec³

2009

Endocrine-Related Cancer

119

107

View full text Add to dashboard Cite

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“…Consistent with this, studies in athymic mice have correlated the increased expression of IL-8 in implanted human CaP cells with increased vascularisation of the tumours and an enhanced tumourigenic and metastatic potential (Inoue et al, 2000;Kim et al, 2001). Other studies have determined the relevance of IL-8 signalling to the development of androgen-independence (Araki et al, 2007;Seaton et al, 2008), CaP cell proliferation (Murphy et al, 2005) and CaP cell survival in response to environmental and chemotherapy/biological agents (Maxwell et al, 2007;Wilson et al, 2008a, b).…”

mentioning

confidence: 85%

Dexamethasone potentiates the antiangiogenic activity of docetaxel in castration-resistant prostate cancer

Wilson¹,

Scullin²,

Worthington³

et al. 2008

Br J Cancer

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We sought to characterise whether dexamethasone (DEX) may enhance tumour response to docetaxel in in vitro and in vivo models of metastatic prostate cancer (CaP). In vitro experiments conducted on PC3 and human bone marrow endothelial cells (hBMECs) determined that administration of DEX (10 nM) reduced constitutive nuclear factor-kB (NF-kB) activity, decreasing interleukin (IL)-8, CXCL1 and VEGF gene expression in PC3 cells. Dexamethasone also attenuated docetaxel-induced NF-kB and activator protein-1 transcription and reduced docetaxel-promoted expression/secretion of IL-8 and CXCL1 in PC3 and hBMECs. Although DEX failed to enhance docetaxel cytotoxicity on PC3 cells, DEX potentiated the antiangiogenic activity of docetaxel in vitro, further reducing vessel area and vessel length in developing endothelial tubes (Po0.05). Docetaxel had a potent antiangiogenic activity in the dorsal skin flap-implanted PC3 tumours in vivo. Small blood vessel formation was further suppressed in tumours co-treated with docetaxel and DEX, substantiated by an increased average vessel diameter and segment length and a decreased number of branch points in the residual tumour vasculature (Po0.001). Our data show that DEX potentiates the antiangiogenic activity of docetaxel, suggesting a putative mechanism for the palliative and survival benefits of these agents in metastatic CaP.

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“…In the context of CaP, CXCL8 expression correlates with increased angiogenesis, tumourigenicity and lymph node metastasis in vivo (Inoue et al, 2000;Kim et al, 2001). We, along with others, have shown that CXCL8 signalling contributes to the transition of a disease to a castration-resistant state (Araki et al, 2007;Seaton et al, 2008). Furthermore, we have shown that CXC-chemokine signalling (including CXCL8) modulates the sensitivity of CaP cells to environmental stresses such as hypoxia and chemotherapy agents, including the DNA-damage agents oxaliplatin and etoposide Wilson et al, 2008a).…”

mentioning

confidence: 72%

Inhibition of constitutive and cxc-chemokine-induced NF-κB activity potentiates ansamycin-based HSP90-inhibitor cytotoxicity in castrate-resistant prostate cancer cells

Seaton¹,

Maxwell²,

Hill³

et al. 2009

Br J Cancer

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BACKGROUND: We determined how CXC-chemokine signalling and necrosis factor-kB (NF-kB) activity affected heat-shock protein 90 (Hsp90) inhibitor (geldanamycin (GA) and 17-allylamino-demethoxygeldanamycin (17-AAG)) cytotoxicity in castrate-resistant prostate cancer (CRPC). METHODS: Geldanamycin and 17-AAG toxicity, together with the CXCR2 antagonist AZ10397767 or NF-kB inhibitor BAY11-7082, was assessed by 3-(4, 5-Dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide assay in two CRPC lines, DU145 and PC3. Flow cytometry quantified apoptotic or necrosis profiles. Necrosis factor-kB activity was determined by luciferase readouts or indirectly by quantitative PCR and ELISA-based determination of CXCL8 expression. RESULTS: Geldanamycin and 17-AAG reduced PC3 and DU145 cell viability, although PC3 cells were less sensitive. Addition of AZ10397767 increased GA (e.g., PC3 IC 20 : from 1.67 ± 0.4 to 0.18 ± 0.2 nM) and 17-AAG (PC3 IC 20 : 43.7 ± 7.8 to 0.64 ± 1.8 nM) potency in PC3 but not DU145 cells. Similarly, BAY11-7082 increased the potency of 17-AAG in PC3 but not in DU145 cells, correlating with the elevated constitutive NF-kB activity in PC3 cells. AZ10397767 increased 17-AAG-induced apoptosis and necrosis and decreased NF-kB activity/CXCL8 expression in 17-AAG-treated PC3 cells. CONCLUSION: Ansamycin cytotoxicity is enhanced by inhibiting NF-kB activity and/or CXC-chemokine signalling in CRPC cells. Detecting and/or inhibiting NF-kB activity may aid the selection and treatment response of CRPC patients to Hsp90 inhibitors.

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Interleukin-8 signaling promotes androgen-independent proliferation of prostate cancer cells via induction of androgen receptor expression and activation

Cited by 125 publications

References 32 publications

Emerging roles of chemokines in prostate cancer

Emerging roles of chemokines in prostate cancer

Dexamethasone potentiates the antiangiogenic activity of docetaxel in castration-resistant prostate cancer

Inhibition of constitutive and cxc-chemokine-induced NF-κB activity potentiates ansamycin-based HSP90-inhibitor cytotoxicity in castrate-resistant prostate cancer cells

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