scholarly journals Paracrine factors produced by bone marrow stromal cells induce apoptosis and neuroendocrine differentiation in prostate cancer cells

The Prostate ◽  
2010 ◽  
Vol 71 (2) ◽  
pp. 157-167 ◽  
Author(s):  
Chu Zhang ◽  
Mehrnoosh Soori ◽  
Fayth L. Miles ◽  
Robert A. Sikes ◽  
Daniel D. Carson ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Bone Marrow ◽  
Cancer Cells ◽  
Stromal Cells ◽  
Bone Marrow Stromal Cells ◽  
Neuroendocrine Differentiation ◽  
Marrow Stromal Cells ◽  
Prostate Cancer Cells ◽  
Paracrine Factors

Human Bone Marrow Stromal Cells Protect Prostate Cancer Cells From TRAIL-Induced Apoptosis

2004 ◽  
Vol 19 (10) ◽  
pp. 1712-1721 ◽  
Author(s):  
Rachel Nyambo ◽  
Neil Cross ◽  
Jenny Lippitt ◽  
Ingunn Holen ◽  
Gorden Bryden ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Bone Marrow ◽  
Cancer Cells ◽  
Stromal Cells ◽  
Bone Marrow Stromal Cells ◽  
Marrow Stromal Cells ◽  
Human Bone ◽  
Human Bone Marrow ◽  
Prostate Cancer Cells ◽  
Induced Apoptosis

scholarly journals Long non‐coding RNA NORAD promotes the prostate cancer cell extracellular vesicle release via microRNA-541-3p-regulated PKM2 to induce bone metastasis of prostate cancer

2021 ◽  
Vol 40 (1) ◽  
Author(s):  
Chuan-yi Hu ◽  
Juan Chen ◽  
Xin-hua Qin ◽  
Pan You ◽  
Jie Ma ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Bone Marrow ◽  
Bone Metastasis ◽  
Stromal Cells ◽  
Bone Marrow Stromal Cells ◽  
Marrow Stromal Cells ◽  
Downstream Target ◽  
Non Coding Rna ◽  
Target Molecules ◽  
Long Non Coding Rna

Abstract Background Bone metastasis is the leading cause of mortality and reduced quality of life in patients with metastatic prostate cancer (PCa). Long non-coding RNA activated by DNA damage (NORAD) has been observed to have an abnormal expression in various cancers. This article aimed to explore the molecular mechanism underlying the regulatory role of NORAD in bone metastasis of PCa. Methods NORAD expression in clinical PCa tissues and cell lines was detected with the application of qRT-PCR. Cancer cells were then transfected with plasmids expressing NORAD, after which Transwell assay and CCK-8 assay were carried out to detect proliferation, migration, and bone metastasis of PCa. NORAD downstream target molecules were screened through bioinformatics analysis, followed by further verification using dual luciferase assay. Extracellular vesicles (EVs) were labeled with PKH67 and interacted with bone marrow stromal cells. The gain- and loss-function method was applied to determine the internalization and secretion of PCa cells-derived EVs under the intervention of downstream target molecules or NORAD. Results PCa tissues and cell lines were observed to have a high expression of NORAD, particularly in tissues with bone metastasis. NORAD knockdown resulted in reduced secretion and internalization of EVs, and suppressed proliferation, migration, and bone metastasis of PCa cells. It was indicated that NORAD interacted with miR-541-3p, leading to the upregulation of PKM2. Forced expression of PKM2 promoted the transfer of PKH67-labeled EVs to bone marrow stromal cells. Conclusions NORAD might serve as a ceRNA of miR-541-3p to promote PKM2 expression, thereby enhancing the development of bone metastasis in PCa by promoting internalization and transfer of EVs of cancer cells, providing an insight into a novel treatment for the disorder.

Bone marrow stromal cells promote growth and survival of prostate cancer cells

2007 ◽  
Vol 35 (4) ◽  
pp. 698-700 ◽  
Author(s):  
N.A. Cross ◽  
M. Papageorgiou ◽  
C.L. Eaton
Keyword(s):  
Prostate Cancer ◽  
Bone Marrow ◽  
Stromal Cells ◽  
Bone Marrow Stromal Cells ◽  
Marrow Stromal Cells ◽  
Cancer Cell Proliferation ◽  
Growth And Survival ◽  
Prostate Cancers ◽  
Necrosis Factor ◽  
Insulin Like Growth Factors

Prostate cancers frequently metastasize to the skeleton, and it has been hypothesized that this environment selectively supports the growth of these tumours. Specifically there is strong evidence that interactions between tumour cells and BMSCs (bone marrow stromal cells) play a major role in supporting prostate cancer growth and survival in bone. Here, we examine factors shown to be secreted by BMSCs, such as IGFs (insulin-like growth factors) and IL-6 (interleukin 6), shown to promote prostate cancer cell proliferation and to potentially replace the requirement for androgens. In addition we discuss another factor produced by BMSCs, osteoprotegerin, which may promote tumour cell survival by suppressing the biological activity of the pro-apoptotic ligand TRAIL (tumour-necrosis-factor-related apoptosis-inducing ligand).

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