Interleukin-17 induces expression of chemokines and cytokines in prostatic epithelial cells but does not stimulate cell growth in vitro

Zongbing You, Dongxia Ge, Sen Liu, Qiuyang Zhang, Alexander D Borowsky, Jonathan Melamed

Research output: Chapter in Book/Report/Conference proceedingChapter

Abstract

Background. Interleukin-17 (IL-17A) expression is increased in prostate cancer. This study investigated the expression of IL-17A receptor C (IL-17RC) in prostatic intraepithelial neoplasia (PIN) lesions and the effects of IL-17A on prostatic epithelial cells in in-vitro studies. Methods. IL-17RC expression in human and rodent prostate tissues was detected by immunohistochemistry. Quantitative real-time reverse-transcription polymerase chain reaction (qRT-PCR) and Western blot analyses were used to determine mRNA and protein expression in human and mouse prostatic epithelial cell lines. Results. IL-17RC protein was increased in human and rodent PIN lesions, compared to the normal human and rodent prostatic epithelium. IL-17A treatment activated the Nuclear Factor-κB (NF-κB) and/or Extracellular signal-Regulated Kinase (ERK) pathways in human PIN and LNCaP cell lines as well as mouse prostate cancer cell line TRAMP-C1. IL-17A treatment did not affect cell growth of the cell lines studied. However, IL-17A induced expression of CXCL1, CXCL2, CCL2, CCL5, and IL-6 in human and mouse prostatic epithelial cell lines. When the full-length IL-17RC was overexpressed in human PIN and LNCaP cell lines, activation of NF-κB and/or ERK pathways and expression of CXCL1, CXCL2, and CCL5 chemokines were significantly enhanced upon IL-17A treatment. Conclusion. These findings suggest that the prostatic epithelial cells in PIN lesions may respond to IL-17A stimuli with augmented synthesis of chemokines, due to increased IL-17RC expression.

Original languageEnglish (US)
Title of host publicationProstate Cancer Cells: Detection, Growth and Treatment
PublisherNova Science Publishers, Inc.
Pages41-56
Number of pages16
ISBN (Print)9781622575251
StatePublished - Dec 2012

Fingerprint

Interleukin-17
Cell growth
Chemokines
Epithelial Cells
Cytokines
Prostatic Intraepithelial Neoplasia
Growth
Cell Line
Cells
Rodentia
Complement Factor B
Extracellular Signal-Regulated MAP Kinases
In Vitro Techniques
Prostatic Neoplasms
Chemokine CXCL1
Chemokine CXCL2
Chemokine CCL5
Polymerase chain reaction
Transcription
Protein C

Keywords

  • Il-17
  • Pin
  • Prostate cancer

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)
  • Medicine(all)

Cite this

You, Z., Ge, D., Liu, S., Zhang, Q., Borowsky, A. D., & Melamed, J. (2012). Interleukin-17 induces expression of chemokines and cytokines in prostatic epithelial cells but does not stimulate cell growth in vitro. In Prostate Cancer Cells: Detection, Growth and Treatment (pp. 41-56). Nova Science Publishers, Inc..

Interleukin-17 induces expression of chemokines and cytokines in prostatic epithelial cells but does not stimulate cell growth in vitro. / You, Zongbing; Ge, Dongxia; Liu, Sen; Zhang, Qiuyang; Borowsky, Alexander D; Melamed, Jonathan.

Prostate Cancer Cells: Detection, Growth and Treatment. Nova Science Publishers, Inc., 2012. p. 41-56.

Research output: Chapter in Book/Report/Conference proceedingChapter

You, Z, Ge, D, Liu, S, Zhang, Q, Borowsky, AD & Melamed, J 2012, Interleukin-17 induces expression of chemokines and cytokines in prostatic epithelial cells but does not stimulate cell growth in vitro. in Prostate Cancer Cells: Detection, Growth and Treatment. Nova Science Publishers, Inc., pp. 41-56.
You Z, Ge D, Liu S, Zhang Q, Borowsky AD, Melamed J. Interleukin-17 induces expression of chemokines and cytokines in prostatic epithelial cells but does not stimulate cell growth in vitro. In Prostate Cancer Cells: Detection, Growth and Treatment. Nova Science Publishers, Inc. 2012. p. 41-56
You, Zongbing ; Ge, Dongxia ; Liu, Sen ; Zhang, Qiuyang ; Borowsky, Alexander D ; Melamed, Jonathan. / Interleukin-17 induces expression of chemokines and cytokines in prostatic epithelial cells but does not stimulate cell growth in vitro. Prostate Cancer Cells: Detection, Growth and Treatment. Nova Science Publishers, Inc., 2012. pp. 41-56
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abstract = "Background. Interleukin-17 (IL-17A) expression is increased in prostate cancer. This study investigated the expression of IL-17A receptor C (IL-17RC) in prostatic intraepithelial neoplasia (PIN) lesions and the effects of IL-17A on prostatic epithelial cells in in-vitro studies. Methods. IL-17RC expression in human and rodent prostate tissues was detected by immunohistochemistry. Quantitative real-time reverse-transcription polymerase chain reaction (qRT-PCR) and Western blot analyses were used to determine mRNA and protein expression in human and mouse prostatic epithelial cell lines. Results. IL-17RC protein was increased in human and rodent PIN lesions, compared to the normal human and rodent prostatic epithelium. IL-17A treatment activated the Nuclear Factor-κB (NF-κB) and/or Extracellular signal-Regulated Kinase (ERK) pathways in human PIN and LNCaP cell lines as well as mouse prostate cancer cell line TRAMP-C1. IL-17A treatment did not affect cell growth of the cell lines studied. However, IL-17A induced expression of CXCL1, CXCL2, CCL2, CCL5, and IL-6 in human and mouse prostatic epithelial cell lines. When the full-length IL-17RC was overexpressed in human PIN and LNCaP cell lines, activation of NF-κB and/or ERK pathways and expression of CXCL1, CXCL2, and CCL5 chemokines were significantly enhanced upon IL-17A treatment. Conclusion. These findings suggest that the prostatic epithelial cells in PIN lesions may respond to IL-17A stimuli with augmented synthesis of chemokines, due to increased IL-17RC expression.",
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T1 - Interleukin-17 induces expression of chemokines and cytokines in prostatic epithelial cells but does not stimulate cell growth in vitro

AU - You, Zongbing

AU - Ge, Dongxia

AU - Liu, Sen

AU - Zhang, Qiuyang

AU - Borowsky, Alexander D

AU - Melamed, Jonathan

PY - 2012/12

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N2 - Background. Interleukin-17 (IL-17A) expression is increased in prostate cancer. This study investigated the expression of IL-17A receptor C (IL-17RC) in prostatic intraepithelial neoplasia (PIN) lesions and the effects of IL-17A on prostatic epithelial cells in in-vitro studies. Methods. IL-17RC expression in human and rodent prostate tissues was detected by immunohistochemistry. Quantitative real-time reverse-transcription polymerase chain reaction (qRT-PCR) and Western blot analyses were used to determine mRNA and protein expression in human and mouse prostatic epithelial cell lines. Results. IL-17RC protein was increased in human and rodent PIN lesions, compared to the normal human and rodent prostatic epithelium. IL-17A treatment activated the Nuclear Factor-κB (NF-κB) and/or Extracellular signal-Regulated Kinase (ERK) pathways in human PIN and LNCaP cell lines as well as mouse prostate cancer cell line TRAMP-C1. IL-17A treatment did not affect cell growth of the cell lines studied. However, IL-17A induced expression of CXCL1, CXCL2, CCL2, CCL5, and IL-6 in human and mouse prostatic epithelial cell lines. When the full-length IL-17RC was overexpressed in human PIN and LNCaP cell lines, activation of NF-κB and/or ERK pathways and expression of CXCL1, CXCL2, and CCL5 chemokines were significantly enhanced upon IL-17A treatment. Conclusion. These findings suggest that the prostatic epithelial cells in PIN lesions may respond to IL-17A stimuli with augmented synthesis of chemokines, due to increased IL-17RC expression.

AB - Background. Interleukin-17 (IL-17A) expression is increased in prostate cancer. This study investigated the expression of IL-17A receptor C (IL-17RC) in prostatic intraepithelial neoplasia (PIN) lesions and the effects of IL-17A on prostatic epithelial cells in in-vitro studies. Methods. IL-17RC expression in human and rodent prostate tissues was detected by immunohistochemistry. Quantitative real-time reverse-transcription polymerase chain reaction (qRT-PCR) and Western blot analyses were used to determine mRNA and protein expression in human and mouse prostatic epithelial cell lines. Results. IL-17RC protein was increased in human and rodent PIN lesions, compared to the normal human and rodent prostatic epithelium. IL-17A treatment activated the Nuclear Factor-κB (NF-κB) and/or Extracellular signal-Regulated Kinase (ERK) pathways in human PIN and LNCaP cell lines as well as mouse prostate cancer cell line TRAMP-C1. IL-17A treatment did not affect cell growth of the cell lines studied. However, IL-17A induced expression of CXCL1, CXCL2, CCL2, CCL5, and IL-6 in human and mouse prostatic epithelial cell lines. When the full-length IL-17RC was overexpressed in human PIN and LNCaP cell lines, activation of NF-κB and/or ERK pathways and expression of CXCL1, CXCL2, and CCL5 chemokines were significantly enhanced upon IL-17A treatment. Conclusion. These findings suggest that the prostatic epithelial cells in PIN lesions may respond to IL-17A stimuli with augmented synthesis of chemokines, due to increased IL-17RC expression.

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