Expression of CCL5 (RANTES) and CCR5 in prostate cancer

Vaday, Gayle G.; Peehl, Donna M.; Kadam, Pournima; Lawrence, Diana M.

doi:10.1002/pros.20306

Cited by 213 publications

(203 citation statements)

References 41 publications

Supporting

Mentioning

189

Contrasting

Unclassified

Order By: Relevance

“…CCR2 expression has been correlated with Gleason grade and pathological stages of PCa and has also been suggested to contribute to PCa development, 32 while CCR5 has been shown to mediate PCa cell proliferation and invasion (albeit when activated by RANTES). 33 Consequently, our data demonstrate that the induction of inflammation in the AROMϩ mouse may facilitate the development of PCa via the altered expression of key cytokines and chemokines, specifically CCL20, CCL8, CCR6, CCR5, and CCR2.…”

Section: Estrogens Prostatitismentioning

confidence: 66%

See 1 more Smart Citation

Increased Endogenous Estrogen Synthesis Leads to the Sequential Induction of Prostatic Inflammation (Prostatitis) and Prostatic Pre-Malignancy

Ellem

Wang

Poutanen

et al. 2009

The American Journal of Pathology

View full text Add to dashboard Cite

Prostatitis causes substantial morbidity to men, through associated urinary symptoms, sexual dysfunction, and pelvic pain; however, 90% to 95% of cases have an unknown etiology. Inflammation is associated with the development of carcinoma, and, therefore, it is imperative to identify and study the causes of prostatitis to improve our understanding of this disease and its role in prostate cancer. As estrogens cause prostatic inflammation, here we characterize the murine prostatic phenotype induced by elevated endogenous estrogens due to aromatase overexpression (AROM؉). Early-life development of the AROM؉ prostate was normal; however, progressive changes culminated in chronic inflammation and pre-malignancy. The AROM؉ prostate was smaller at puberty compared with wild-type controls. Mast cell numbers were significantly increased at puberty and preceded chronic inflammation, which emerged by 40 weeks of age and was characterized by increased mast cell, macrophage, neutrophil, and T-lymphocyte numbers. The expression of key inflammatory mediators was also significantly altered, and premalignant prostatic intraepithelial neoplasia lesions emerged by 52 weeks of age. Taken together, these data link estrogens to prostatitis and premalignancy in the prostate, further implicating a role for estrogen in prostate cancer. These data also establish the AROM؉ mouse as a novel, non-bacterial model for the study of prostatitis. Prostatitis, an exceedingly common condition in the male population worldwide, has an incidence of ϳ9% and a prevalence of ϳ14%, and, unlike benign prostatic hyperplasia and prostate cancer (PCa), which are predominantly diseases of older men, prostatitis afflicts men of all ages. It is also the most common outpatient condition seen in men under 50 years of age and accounts for more clinical visits than either PCa and/or benign prostatic hyperplasia.1,2 At present our knowledge of prostatitis is lacking, with 90% to 95% of cases having an unknown etiology. This represents a significant problem, particularly as prostatitis has also been implicated in the development of PCa.3-5 Given the prevalence of prostatitis and this putative link to PCa, it is vitally important to identify the unknown causes of prostatitis.Several causes of prostatitis have been postulated, including hormonal variation or exposure, infection due to sexually transmitted disease, 6 dietary factors, and physical trauma from urine reflux. 7 However, of particular interest is an apparent link between estrogen and prostatic inflammation, 8 which has emerged mainly from the administration of pharmacological levels of exogenous estrogen to rodents.9 Additional data obtained from further rodent studies show that the prostate gland is particularly sensitive to estrogenic exposure during development in fetal and neonatal life; transient estrogen exposure before puberty results in inflammation later in life, well after the exposure has occurred.10,11 Several decades of research from various laboratories, including our own, has demonstrated that...

show abstract

Section: Estrogens Prostatitismentioning

confidence: 66%

“…Of particular significance were significant increases in the expression of CCL20, CCL8, CCR6, CCR5, and CCR2, all of which have been implicated in the development of PCa. 31,32,33 …”

Section: Chronic Inflammation As a Cause Of Prostatic Premalignancymentioning

confidence: 99%

Increased Endogenous Estrogen Synthesis Leads to the Sequential Induction of Prostatic Inflammation (Prostatitis) and Prostatic Pre-Malignancy

Ellem

Wang

Poutanen

et al. 2009

The American Journal of Pathology

View full text Add to dashboard Cite

show abstract

“…Initially, IL-8 and RANTES were identified for their ability to stimulate migration of proinflammatory cells [44]. Recent studies demonstrated that these chemokines have broader biological effects and are able to stimulate proliferation of malignant and endothelial cells to stimulate tumor blood vessel network formation [45][46][47][48] and increased blood levels of IL-8 and RANTES is often associated with poor prognosis in cancer patients [46][47][48].…”

Section: Discussionmentioning

confidence: 99%

Multiple effects of TRAIL in human carcinoma cells: Induction of apoptosis, senescence, proliferation, and cytokine production

Levina

Marrangoni

DeMarco

et al. 2008

Experimental Cell Research

View full text Add to dashboard Cite

TRAIL is a death ligand that induces apoptosis in malignant but not normal cells. Recently the ability of TRAIL to induce proliferation in apoptosis-resistant normal and malignant cells was reported. In this study, we analyzed TRAIL effects in apoptosis sensitive MCF7, OVCAR3 and H460 human tumor cell lines. TRAIL at low concentrations preferentially induced cell proliferation. At 100 ng/ ml apoptotic death was readily observed, however surviving cells acquired higher proliferative capacity. TRAIL stimulated production of several cytokines, IL-8, RANTES, MCP-1 and bFGF, and activation of caspases 1 and 8 was essential for this effect. Antibodies to IL-8, RANTES, and bFGF blocked TRAIL-induced cell proliferation and further stimulated apoptosis. For the first time, we report that high TRAIL concentrations induced cell senescence as determined by altered morphology and expression of several senescence markers: SA-β-gal, p21 Waf1/Cip1 , p16 INK4a , and HMGA. Caspase 9 inhibition protected TRAIL-treated cells from senescence, whereas inhibition of caspases 1 and 8 increased yield of SLP cells. In conclusion, in cultured human carcinoma cells, TRAIL therapy results in three functional outcomes, apoptosis, proliferation and senescence. TRAIL induced proapoptotic and prosurvival responses correlate with strength of signaling. TRAIL-induced cytokine production is responsible for its proliferative and prosurvival effects.

show abstract

“…Co-expression of CCR4 and CCR10, the known pair of skinhoming chemokine receptors, may play an important role in adult T-cell leukemia/ lymphoma (ATLL) invasion into the skin [177]. CCL5 and its receptor CCR5 has been detected on prostate cancer cell lines [178]. CCR6 and its ligand have been shown to be involved in colorectal cancer and its metastasis [179]; CCR9 on prostate and melanoma cells [180,181]; and CCR10 on melanoma cells [133].…”

Section: Chemokines and Their Receptors In Tumor Growth And Metastasismentioning

confidence: 99%

Chemokines in tumor angiogenesis and metastasis

Singh

Sadanandam

Singh

2007

Cancer Metastasis Rev

158

132

View full text Add to dashboard Cite

Chemokines are a large group of low molecular weight cytokines that are known to selectively attract and activate different cell types. Although the primary function of chemokines is well recognized as leukocyte attractants, recent evidences indicate that they also play a role in number of tumor-related processes, such as growth, angiogenesis and metastasis. Chemokines activate cells through cell surface seven trans-membranes, G-protein-coupled receptors (GPCR). The role played by chemokines and their receptors in tumor pathophysiology is complex as some chemokines favor tumor growth and metastasis, while others may enhance anti-tumor immunity. These diverse functions of chemokines establish them as key mediators between the tumor cells and their microenvironment and play critical role in tumor progression and metastasis. In this review, we present some of the recent advances in chemokine research with special emphasis on its role in tumor angiogenesis and metastasis.

show abstract

Expression of CCL5 (RANTES) and CCR5 in prostate cancer

Cited by 213 publications

References 41 publications

Increased Endogenous Estrogen Synthesis Leads to the Sequential Induction of Prostatic Inflammation (Prostatitis) and Prostatic Pre-Malignancy

Increased Endogenous Estrogen Synthesis Leads to the Sequential Induction of Prostatic Inflammation (Prostatitis) and Prostatic Pre-Malignancy

Multiple effects of TRAIL in human carcinoma cells: Induction of apoptosis, senescence, proliferation, and cytokine production

Chemokines in tumor angiogenesis and metastasis

Contact Info

Product

Resources

About