scholarly journals Somatic aberrations of BRCA1 gene are associated with ALDH1, EGFR, and tumor progression in prostate cancer

2018 ◽  
Vol 144 (3) ◽  
pp. 607-614 ◽  
Author(s):  
Aleksandra Omari ◽  
Paulina Nastały ◽  
Sara Stoupiec ◽  
Aneta Bałabas ◽  
Michalina Dąbrowska ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Tumor Progression ◽  
Brca1 Gene ◽  
Somatic Aberrations

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

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

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

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.

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

Cancers ◽  
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.

2137 EXPRESSION OF ESTROGEN RELATED PROTEINS IN HORMONE-REFRACTORY PROSTATE CANCER: ASSOCIATION WITH TUMOR PROGRESSION

2010 ◽  
Vol 183 (4S) ◽  
Author(s):  
Olivier Celhay ◽  
Mokrane Yacoub ◽  
Bertrand Doré ◽  
Jacques Irani ◽  
Olivier Cussenot ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Tumor Progression ◽  
Hormone Refractory Prostate Cancer ◽  
Hormone Refractory ◽  
Related Proteins

scholarly journals Real-time monitoring of tumor progression and drug responses in a preclinical mouse model of prostate cancer

Oncotarget ◽  
2016 ◽  
Vol 7 (22) ◽  
pp. 33025-33034 ◽  
Author(s):  
Peng Xu ◽  
Naijin Xu ◽  
Kai Guo ◽  
Abai Xu ◽  
Fumiaki Takenaka ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Mouse Model ◽  
Tumor Progression ◽  
Real Time ◽  
Real Time Monitoring ◽  
Drug Responses

Claspin Overexpression Promotes Tumor Progression and Predicts Poor Clinical Outcome in Prostate Cancer

2021 ◽  
Vol 25 (2) ◽  
pp. 131-139 ◽  
Author(s):  
Chao Cai ◽  
Jiexin Luo ◽  
Qinwei Liu ◽  
Zezhen Liu ◽  
Yan Zhao ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Clinical Outcome ◽  
Tumor Progression ◽  
Poor Clinical Outcome

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.

scholarly journals A CTGF‐RUNX2‐RANKL Axis in Breast and Prostate Cancer Cells Promotes Tumor Progression in Bone

2019 ◽  
Vol 35 (1) ◽  
pp. 155-166 ◽  
Author(s):  
Bongjun Kim ◽  
Haemin Kim ◽  
Suhan Jung ◽  
Aree Moon ◽  
Dong‐Young Noh ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Tumor Progression ◽  
Cancer Cells ◽  
Prostate Cancer Cells ◽  
Breast And Prostate Cancer
Sign in / Sign up

Export Citation Format

Share Document