Vasoactive intestinal peptide and pituitary adenylate cyclase activating polypeptide stimulate interleukin-6 production in prostate cancer cells and prostatic epithelial cells

2005 ◽  
Author(s):  
Osamu Nagakawa ◽  
Akira Junicho ◽  
Takuya Akashi ◽  
Keiichi Koizumi ◽  
Tadashi Matsuda ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Epithelial Cells ◽  
Adenylate Cyclase ◽  
Cancer Cells ◽  
Vasoactive Intestinal Peptide ◽  
Interleukin 6 ◽  
Prostate Cancer Cells ◽  
Pituitary Adenylate Cyclase

Basal prostate epithelial cells stimulate the migration of prostate cancer cells

2004 ◽  
Vol 41 (2) ◽  
pp. 85-97 ◽  
Author(s):  
Hsiao-Man Yu ◽  
Diane E. Frank ◽  
Jie Zhang ◽  
Xueke You ◽  
William G. Carter ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Epithelial Cells ◽  
Cancer Cells ◽  
Prostate Cancer Cells ◽  
Prostate Epithelial Cells

AT‐rich interaction domain 5A regulates the transcription of interleukin‐6 gene in prostate cancer cells

The Prostate ◽  
2021 ◽  
Author(s):  
Wataru Ikeuchi ◽  
Yuriko Wakita ◽  
Guoxiang Zhang ◽  
Chun Li ◽  
Keiichi Itakura ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cancer Cells ◽  
Interleukin 6 ◽  
Prostate Cancer Cells ◽  
Interaction Domain ◽  
Rich Interaction

1291 INTERLEUKIN-6 REGULATES INTRACRINE ANDROGEN SYNTHESIS IN PROSTATE CANCER CELLS

2010 ◽  
Vol 183 (4S) ◽  
Author(s):  
Jae Chun ◽  
Nagalskshmi Nadiminty ◽  
Wei Lou ◽  
Christopher Evans ◽  
Allen Gao
Keyword(s):  
Prostate Cancer ◽  
Cancer Cells ◽  
Interleukin 6 ◽  
Prostate Cancer Cells ◽  
Androgen Synthesis

Regulation of growth of prostate cancer cells selected in the presence of interleukin-6 by the anti-interleukin-6 antibody CNTO 328

The Prostate ◽  
2006 ◽  
Vol 66 (16) ◽  
pp. 1744-1752 ◽  
Author(s):  
Hannes Steiner ◽  
Ilaria T. Cavarretta ◽  
Patrizia L. Moser ◽  
Andreas P. Berger ◽  
Jasmin Bektic ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cancer Cells ◽  
Interleukin 6 ◽  
Prostate Cancer Cells ◽  
Regulation Of Growth

scholarly journals Regenerated Luminal Epithelial Cells Are Derived from Preexisting Luminal Epithelial Cells in Adult Mouse Prostate

2011 ◽  
Vol 25 (11) ◽  
pp. 1849-1857 ◽  
Author(s):  
June Liu ◽  
Laura E. Pascal ◽  
Sudhir Isharwal ◽  
Daniel Metzger ◽  
Raquel Ramos Garcia ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Epithelial Cells ◽  
Cancer Cells ◽  
Androgen Deprivation Therapy ◽  
Specific Antigen ◽  
Androgen Deprivation ◽  
Genetic Lineage ◽  
Prostate Cancer Cells ◽  
Mouse Prostate ◽  
Luminal Epithelial Cells

Abstract Determining the source of regenerated luminal epithelial cells in the adult prostate during androgen deprivation and replacement will provide insights into the origin of prostate cancer cells and their fate during androgen deprivation therapy. Prostate stem cells in the epithelial layer have been suggested to give rise to luminal epithelium. However, the extent of stem cell participation to prostate regrowth is not clear. In this report, using prostate-specific antigen-CreERT2-based genetic lineage marking/tracing in mice, preexisting luminal epithelial cells were shown to be a source of regenerated luminal epithelial cells in the adult prostate. Prostatic luminal epithelial cells could survive androgen deprivation and were capable of proliferating upon androgen replacement. Prostate cancer cells, typically exhibiting a luminal epithelial phenotype, may retain this intrinsic capability to survive and regenerate in response to changes in androgen signaling, providing part of the mechanism for the ultimate failure of androgen deprivation therapy in prostate cancer.

Effect of androgen signaling in stromal cells on growth of prostate cancer.

2016 ◽  
Vol 34 (2_suppl) ◽  
pp. 297-297 ◽  
Author(s):  
Chun-Peng Liao ◽  
Leng-Ying Chen ◽  
Andrea Luethy ◽  
Youngsoo Kim ◽  
A. Robert MacLeod ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Epithelial Cells ◽  
Cancer Cells ◽  
Stromal Cells ◽  
Culture System ◽  
Human Prostate ◽  
Human Prostate Cancer ◽  
Prostate Cancer Cells ◽  
Epithelial Cancer ◽  
Mesenchymal Transition

297 Background: Interactions between epithelial and stroma cells are important in the development of prostate cancer (PCa). Cancer-associated fibroblasts (CAFs) have been to support tumor progression, metastasis, and differentiation. Androgen receptor (AR) and related pathways are known to support the growth and survival of prostate epithelial cancer cells, the roles of AR-dependent processes in cancerous stroma are less clear. We sought to investigate if AR-dependent pathways present in CAF cells influence the growth and tumorogencity of epithelial cancer cells in relation to androgen-deprivation therapy in prostate cancer. Methods: Murine CAFs were isolated from a well-described PTEN-dependent cancer mouse model (Liao, et al Cancer Res, 2010. 70(18):7294). A co-culture system was developed based on multiple lines of murine CAFs grown along with human prostate cancer epithelial cells, and a murine-specific anti-sense oligonucleotide (ASO) against murine AR was used to specifically suppress AR expression in murine CAFs in this system. RT-PCR was used to investigate changes in gene expression. Results: Using this co-culture system, we found that murine CAFs promoted cell proliferation and colony formation in several human prostate cancer cell lines. Further, these processes were decreased by suppression of AR-expression in CAFs. Expression of genes related to tumorigenicity in epithelial cells were investigated. Markers associated with epithelial-mesenchymal transition (EMT, N-Cad) and “stemness” (OCT4, Sox2, Nanog) were increased in human prostate cancer cells grown with low-AR CAFs. Conclusions: Our data indicates that suppression of AR in CAFs results in down-regulation in the growth and tumorigenicity of prostate cancer cells through pathways related to EMT and “cell reprograming”. As such, development of therapies which inhibit the tumor-promoting pathways present in stromal cells may be one approach to improve the treatment of prostate cancer.

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