scholarly journals MicroRNA-466 inhibits tumor growth and bone metastasis in prostate cancer by direct regulation of osteogenic transcription factor RUNX2

2017 ◽  
Vol 8 (1) ◽  
pp. e2572-e2572 ◽  
Author(s):  
Melissa Colden ◽  
Altaf A Dar ◽  
Sharanjot Saini ◽  
Priya V Dahiya ◽  
Varahram Shahryari ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Transcription Factor ◽  
Bone Metastasis ◽  
Tumor Growth ◽  
Direct Regulation

KLF9, a transcription factor induced in flutamide-caused cell apoptosis, inhibits AKT activation and suppresses tumor growth of prostate cancer cells

The Prostate ◽  
2014 ◽  
Vol 74 (9) ◽  
pp. 946-958 ◽  
Author(s):  
Pengliang Shen ◽  
Jiabin Sun ◽  
Guiqin Xu ◽  
Li Zhang ◽  
Zhaojuan Yang ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Transcription Factor ◽  
Tumor Growth ◽  
Cancer Cells ◽  
Cell Apoptosis ◽  
Prostate Cancer Cells ◽  
Akt Activation

scholarly journals Pristimerin Inhibits Prostate Cancer Bone Metastasis by Targeting PC-3 Stem Cell Characteristics and VEGF-Induced Vasculogenesis of BM-EPCs

2015 ◽  
Vol 37 (1) ◽  
pp. 253-268 ◽  
Author(s):  
Shuai Huang ◽  
Peiheng He ◽  
Xinsheng Peng ◽  
Jinglei Li ◽  
Dongliang Xu ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Stem Cell ◽  
Bone Metastasis ◽  
Protein Expression ◽  
Tumor Growth ◽  
Metastatic Progression ◽  
Mice Model ◽  
Spheroid Formation ◽  
Angiogenic Switch

Background/Aims: Prostate cancer (PCa) is one of the most common malignant cancers and a major leading cause of cancer deaths in men. Cancer stem-like cells are shown to be highly tumorigenic, pro-angiogenic and can significantly contribute to tumor new vessel formation and bone marrow derived-EPCs (BM-EPCs) are shown to recruit to the angiogenic switch in tumor growth and metastatic progression, suggesting the importance of targeting cancer stem cells (CSCs) and EPCs for novel tumor therapies. Pristimerin, an active component isolated from Celastraceae and Hippocrateaceae, has shown anti-tumor effects in some cell lines in previous studies. However, the effect and mechanism of Pristimerin on CSCs and EPCs in PCa bone metastasis are not well studied. Methods: The effect of Pristimerin on PC-3 stem cell characteristics and metastasis were detected by spheroid formation, CD133 and CD44 protein expression, matrix-gel invasive assay and colony-formation assay in vitro, VEGF and pro-inflammatory cytokines expression by ELISA assay, and tumor tumorigenicity by X-ray and MR in NOD-SCID mice model in vivo. In addition, we also detected the effect of Pristimerin on VEGF-induced vasculogenesis and protein expression of BM-EPCs. Results: Pristimerin could significantly inhibit spheroid formation and protein expression of CD133 and CD44, reduce VEGF and pro-inflammation cytokines expression of PC-3 cell, and prevent the xenografted PC-3 tumor growth in the bone of nude mice. The present data also showed that Pristimerin significantly inhibited VEGF-induced vasculogenesis of BM-EPCs by suppressing the EPCs functions including proliferation, adhesion, migration, tube formation and inactivation the phosphorylation of VEGFR-2, Akt and eNOS. Conclusion: These data provide evidence that Pristimerin has strong potential for development as a novel agent against prostate bone metastasis by suppressing PC-3 stem cell characteristics and VEGF-induced vasculogenesis of BM-EPCs.

scholarly journals Acetylation of KLF5 maintains EMT and tumorigenicity to cause chemoresistant bone metastasis in prostate cancer

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Baotong Zhang ◽  
Yixiang Li ◽  
Qiao Wu ◽  
Lin Xie ◽  
Benjamin Barwick ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Transcription Factor ◽  
Bone Metastasis ◽  
Bone Metastases ◽  
Advanced Prostate Cancer ◽  
Paracrine Signaling ◽  
Mesenchymal Phenotype ◽  
Cxcr4 Signaling ◽  
Metastatic Lesions ◽  
Underlying Mechanisms

AbstractAdvanced prostate cancer (PCa) often develops bone metastasis, for which therapies are very limited and the underlying mechanisms are poorly understood. We report that bone-borne TGF-β induces the acetylation of transcription factor KLF5 in PCa bone metastases, and acetylated KLF5 (Ac-KLF5) causes osteoclastogenesis and bone metastatic lesions by activating CXCR4, which leads to IL-11 secretion, and stimulating SHH/IL-6 paracrine signaling. While essential for maintaining the mesenchymal phenotype and tumorigenicity, Ac-KLF5 also causes resistance to docetaxel in tumors and bone metastases, which is overcome by targeting CXCR4 with FDA-approved plerixafor. Establishing a mechanism for bone metastasis and chemoresistance in PCa, these findings provide a rationale for treating chemoresistant bone metastasis of PCa with inhibitors of Ac-KLF5/CXCR4 signaling.

434: Membrane Type-1 Matrix Metalloproteinase (MT1-MMP) Promotes Tumor Growth and Bone Degradation in Prostate Cancer Bone Metastasis

2006 ◽  
Vol 175 (4S) ◽  
pp. 141-141
Author(s):  
R. Daniel Bonfil ◽  
Zhong Dong ◽  
J. Carlos Trindade Filho ◽  
Huiren Zhao ◽  
Pamela Ossenkowski ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Bone Metastasis ◽  
Matrix Metalloproteinase ◽  
Tumor Growth ◽  
Bone Degradation ◽  
Membrane Type

scholarly journals Maspin expression inhibits osteolysis, tumor growth, and angiogenesis in a model of prostate cancer bone metastasis

2003 ◽  
Vol 100 (13) ◽  
pp. 7847-7852 ◽  
Author(s):  
M. L. Cher ◽  
H. R. Biliran ◽  
S. Bhagat ◽  
Y. Meng ◽  
M. Che ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Bone Metastasis ◽  
Tumor Growth ◽  
Maspin Expression

scholarly journals Long Noncoding RNA HOXA11-AS and Transcription Factor HOXB13 Modulate the Expression of Bone Metastasis-Related Genes in Prostate Cancer

Genes ◽  
2021 ◽  
Vol 12 (2) ◽  
pp. 182
Author(s):  
Aya Misawa ◽  
Yukihiro Kondo ◽  
Hiroyuki Takei ◽  
Toshihiro Takizawa
Keyword(s):  
Prostate Cancer ◽  
Transcription Factor ◽  
Bone Metastasis ◽  
Cancer Cells ◽  
Noncoding Rna ◽  
Osteoblastic Cells ◽  
Prostate Cancer Cells ◽  
Upstream Regulator ◽  
Chemokine Ligand ◽  
Pc3 Cells

Long noncoding RNAs (lncRNAs) are emerging as critical regulators of gene expression, which play fundamental roles in cancer development. In this study, we found that homeobox A11 antisense RNA (HOXA11-AS), a highly expressed lncRNA in cell lines derived from prostate cancer bone metastases, promoted the cell invasion and proliferation of PC3 prostate cancer cells. Transcription factor homeobox B13 (HOXB13) was identified as an upstream regulator of HOXA11-AS.HOXA11-AS regulated bone metastasis-associated C-C motif chemokine ligand 2 (CCL2)/C-C chemokine receptor type 2 (CCR2) signaling in both PC3 prostate cancer cells and SaOS2 osteoblastic cells. The HOXB13/HOXA11-AS axis also regulated integrin subunits (ITGAV and ITGB1) specific to prostate cancer bone metastasis. HOXB13, in combination with HOXA11-AS, directly regulated the integrin-binding sialoprotein (IBSP) promoter. Furthermore, conditioned medium containing HOXA11-AS secreted from PC3 cells could induce the expression of CCL2 and IBSP in SaOS2 osteoblastic cells. These results suggest that prostate cancer HOXA11-AS and HOXB13 promote metastasis by regulation of CCL2/CCR2 cytokine and integrin signaling in autocrine and paracrine manners.

466: Age is an Independent Predictor of Bone Metastasis at Prostate Cancer Diagnosis

2007 ◽  
Vol 177 (4S) ◽  
pp. 156-156
Author(s):  
Andrea Salonia ◽  
Pierre I. Karakiewicz ◽  
Andrea Gallina ◽  
Alberto Briganti ◽  
Tommaso C. Camerata ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Bone Metastasis ◽  
Cancer Diagnosis ◽  
Independent Predictor ◽  
Prostate Cancer Diagnosis
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