587: Cxcl14 (BRAK) Expression is Elevated in Prostate Cancer and May Promote Tumor Progression Through Inflammation and Endothelial Cell Recruitment

Vascular endothelial growth factor-A (VEGF) is critical for the development, growth, and survival of blood vessels. Retinal pigmented epithelial (RPE) cells are a major source of VEGF in the retina, with evidence that the extracellular matrix (ECM)-binding forms are particularly important. VEGF associates with fibronectin in the ECM to mediate distinct signals in endothelial cells that are required for full angiogenic activity. Hypoxia stimulates VEGF expression and angiogenesis; however, little is known about whether hypoxia also affects VEGF deposition within the ECM. Therefore, we investigated the role of hypoxia in modulating VEGF-ECM interactions using a primary retinal cell culture model. We found that retinal endothelial cell attachment to RPE cell layers was enhanced in cells maintained under hypoxic conditions. Furthermore, we found that agents that disrupt VEGF-fibronectin interactions inhibited endothelial cell attachment to RPE cells. We also found that hypoxia induced a general change in the chemical structure of the HS produced by the RPE cells, which correlated to changes in the deposition of VEGF in the ECM, and we further identified preferential binding of VEGFR2 over VEGFR1 to VEGF laden-fibronectin matrices. Collectively, these results indicate that hypoxia-induced HS may prime fibronectin for VEGF deposition and endothelial cell recruitment by promoting VEGF-VEGFR2 interactions as a potential means to control angiogenesis in the retina and other tissues.

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150: Inhibition of Tumor Progression Using Antisense Oligonucleotide Targeting GLI2 in Androgen Independent Prostate Cancer

The Journal of Urology ◽

10.1016/s0022-5347(18)30415-4 ◽

2007 ◽

Vol 177 (4S) ◽

pp. 51-51

Author(s):

Shintaro Narita ◽

Alan I. So ◽

Shannon Sinnemann ◽

Ladan Fazli ◽

Eric G. Marcusson ◽

...

Keyword(s):

Prostate Cancer ◽

Tumor Progression ◽

Antisense Oligonucleotide ◽

Androgen Independent

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Apoptosis and Tumor Progression in Prostate Cancer

10.21236/ada467940 ◽

2006 ◽

Author(s):

Martin Tenniswood

Keyword(s):

Prostate Cancer ◽

Tumor Progression

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Lamin B1 promotes tumor progression and metastasis in primary prostate cancer patients

Future Oncology ◽

10.2217/fon-2020-0825 ◽

2020 ◽

Author(s):

Fei Luo ◽

Jiaxi Han ◽

Yatong Chen ◽

Kuo Yang ◽

Zhihua Zhang ◽

...

Keyword(s):

Prostate Cancer ◽

Tumor Progression ◽

Cancer Metastasis ◽

Disease Free Survival ◽

Free Survival ◽

Lamin B1 ◽

Kaplan Meier ◽

Primary Prostate Cancer ◽

Clinical Relationship

Aims: To determine the role of lamin B1 (LMNB1) in the progression and metastasis of primary prostate cancer (PC). Patients & methods: Two PC cohorts were used to investigate the clinical relationship between LMNB1 expression and tumor progression and metastasis. Results: The qRT-PCR results revealed that LMNB1 expression was markedly increased in patients with aggressive features and was associated with worse prognosis. Logistic regression analyses indicated that LMNB1 expression is an independent risk factor for distant metastasis. Kaplan–Meier analysis showed that increased LMNB1 levels were related to poor disease-free survival in the primary PC cohort. Conclusion: This study reveals that upregulation of LMNB1 is associated with cancer metastasis and poor survival outcomes in primary PC patients.

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Cell Plasticity and Prostate Cancer: The Role of Epithelial–Mesenchymal Transition in Tumor Progression, Invasion, Metastasis and Cancer Therapy Resistance

Cancers ◽

10.3390/cancers13112795 ◽

2021 ◽

Vol 13 (11) ◽

pp. 2795

Author(s):

Sofia Papanikolaou ◽

Aikaterini Vourda ◽

Spyros Syggelos ◽

Kostis Gyftopoulos

Keyword(s):

Prostate Cancer ◽

Cancer Therapy ◽

Tumor Progression ◽

Epithelial Mesenchymal Transition ◽

Metastatic Tumor ◽

Therapy Resistance ◽

Cellular Process ◽

Cell Plasticity ◽

Mesenchymal Transition

Prostate cancer, the second most common malignancy in men, is characterized by high heterogeneity that poses several therapeutic challenges. Epithelial–mesenchymal transition (EMT) is a dynamic, reversible cellular process which is essential in normal embryonic morphogenesis and wound healing. However, the cellular changes that are induced by EMT suggest that it may also play a central role in tumor progression, invasion, metastasis, and resistance to current therapeutic options. These changes include enhanced motility and loss of cell–cell adhesion that form a more aggressive cellular phenotype. Moreover, the reverse process (MET) is a necessary element of the metastatic tumor process. It is highly probable that this cell plasticity reflects a hybrid state between epithelial and mesenchymal status. In this review, we describe the underlying key mechanisms of the EMT-induced phenotype modulation that contribute to prostate tumor aggressiveness and cancer therapy resistance, in an effort to provide a framework of this complex cellular process.

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