scholarly journals Specific Binding of Novel SPION-Based System Bearing Anti-N-Cadherin Antibodies to Prostate Tumor Cells

2021 ◽  
Vol Volume 16 ◽  
pp. 6537-6552
Author(s):  
Karolina Karnas ◽  
Tomasz Strączek ◽  
Czesław Kapusta ◽  
Małgorzata Lekka ◽  
Joanna Dulińska-Litewka ◽  
...  
Keyword(s):  
Tumor Cells ◽  
Specific Binding ◽  
Prostate Tumor ◽  
Prostate Tumor Cells

scholarly journals Relationships between proto-oncogene expression and apoptosis induced by anticancer drugs in human prostate tumor cells

1995 ◽  
Vol 1270 (1) ◽  
pp. 12-18 ◽  
Author(s):  
Birandra K. Sinha ◽  
Hiroyuki Yamazaki ◽  
Helen M. Eliot ◽  
Erasmus Schneider ◽  
Markus M. Borner ◽  
...  
Keyword(s):  
Tumor Cells ◽  
Anticancer Drugs ◽  
Prostate Tumor ◽  
Human Prostate ◽  
Oncogene Expression ◽  
Prostate Tumor Cells ◽  
Human Prostate Tumor

scholarly journals Cytoplasmic retention of protein tyrosine kinase 6 promotes growth of prostate tumor cells

Cell Cycle ◽  
2010 ◽  
Vol 9 (20) ◽  
pp. 4190-4199 ◽  
Author(s):  
Patrick M. Brauer ◽  
Yu Zheng ◽  
Lin Wang ◽  
Angela Tyner
Keyword(s):  
Tyrosine Kinase ◽  
Tumor Cells ◽  
Protein Tyrosine Kinase ◽  
Prostate Tumor ◽  
Protein Tyrosine ◽  
Prostate Tumor Cells

The Aryl Propionic Acid R-Flurbiprofen Selectively Induces p75NTR-Dependent Decreased Survival of Prostate Tumor Cells

2007 ◽  
Vol 67 (7) ◽  
pp. 3254-3262 ◽  
Author(s):  
Emily J. Quann ◽  
Fatima Khwaja ◽  
Kenton H. Zavitz ◽  
Daniel Djakiew
Keyword(s):  
Tumor Cells ◽  
Propionic Acid ◽  
Prostate Tumor ◽  
Prostate Tumor Cells

scholarly journals Elevating SOX2 in prostate tumor cells upregulates expression of neuroendocrine genes, but does not reduce the inhibitory effects of enzalutamide

2019 ◽  
Vol 235 (4) ◽  
pp. 3731-3740 ◽  
Author(s):  
Ethan P. Metz ◽  
Phillip J. Wilder ◽  
Jixin Dong ◽  
Kaustubh Datta ◽  
Angie Rizzino
Keyword(s):  
Tumor Cells ◽  
Prostate Tumor ◽  
Inhibitory Effects ◽  
Prostate Tumor Cells

The secreted matrix protein mindin increases prostate tumor progression and tumor-bone crosstalk via ERK 1/2 regulation

2019 ◽  
Vol 40 (7) ◽  
pp. 828-839
Author(s):  
Juan A Ardura ◽  
Irene Gutiérrez-Rojas ◽  
Luis Álvarez-Carrión ◽  
M Rosario Rodríguez-Ramos ◽  
José M Pozuelo ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Tumor Progression ◽  
Tumor Cells ◽  
Matrix Protein ◽  
Bone Cells ◽  
Prostate Tumor ◽  
Dependent Manner ◽  
Prostate Tumors ◽  
Adenocarcinoma Cells ◽  
Prostate Tumor Cells

Abstract Advanced prostate cancer cells preferentially metastasize to bone by acquiring a bone phenotype that allows metastatic cells to thrive in the skeletal environment. Identification of factors that promote the expression of ectopic bone genes—process known as osteomimicry—leading to tumor progression is crucial to prevent and treat metastatic prostate cancer and prolong life expectancy for patients. Here, we identify the extracelular matrix protein mindin in the secretome of prostate adenocarcinoma cells and show that mindin overexpression in human and mouse TRAMP-C1-induced prostate tumors correlates with upregulated levels of bone-related genes in the tumorigenic prostate tissues. Moreover, mindin silencing decreased osteomimicry in adenocarcinoma cells and in the prostate tumor mice model, as well as reduced tumor cell proliferation, migration and adhesion to bone cells. Inhibition of the extracellular signal-regulated kinase 1/2 (ERK 1/2) phosphorylation decreased the proliferative, migratory and pro-adhesion actions of mindin on prostate tumor cells. In addition, conditioned media obtained by crosstalk stimulation of either osteocytes or osteoblasts with the secretome of TRAMP-C1 cells promoted osteomimicry in prostate tumor cells; an effect inhibited by mindin silencing of TRAMP-C1 cells. In vivo, tibiae of primary tumor-bearing mice overexpressed the pro-angiogenic and pro-metastattic factor vascular endothelial growth factor receptor 2 (VEGFR2) in a mindin-dependent manner. Our findings indicate that mindin is a novel regulator of osteomimicry in prostate tumors and potentially mediates tumor-bone cell crosstalk, suggesting its promising role as a target to inhibit bone metastases.

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