Molecular Pathogenesis and Progression of Prostate Cancer

Schrecengost, Randy S.; Knudsen, Karen E.

doi:10.1053/j.seminoncol.2013.04.001

Cited by 99 publications

(103 citation statements)

References 138 publications

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“…Progression toward metastatic castrate-resistant prostate cancer and the contribution of aberrant androgen signaling to this process remain a major therapeutic challenge (38). Negative androgen receptor (AR) status is correlated with the expression of Endo180 in breast cancer (7).…”

Section: Discussionmentioning

confidence: 99%

Survival Outcome and EMT Suppression Mediated by a Lectin Domain Interaction of Endo180 and CD147

Rodriguez-Teja

Gronau

Minamidate

et al. 2015

Molecular Cancer Research

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Epithelial cell-cell contacts maintain normal glandular tissue homeostasis, and their breakage can trigger epithelialto-mesenchymal transition (EMT), a fundamental step in the development of metastatic cancer. Despite the ability of C-type lectin domains (CTLD) to modulate cell-cell adhesion, it is not known if they modulate epithelial adhesion in EMT and tumor progression. Here, the multi-CTLD mannose receptor, Endo180 (MRC2/uPARAP), was shown using the Kaplan-Meier analysis to be predictive of survival outcome in men with early prostate cancer. A proteomic screen of novel interaction partners with the fourth CTLD (CTLD4) in Endo180 revealed that its complex with CD147 is indispensable for the stability of three-dimensional acini formed by nontransformed prostate epithelial cells (PEC). Mechanistic study using knockdown of Endo180 or CD147, and treatment with an Endo180 mAb targeting CTLD4 (clone 39.10), or a dominant-negative GST-CTLD4 chimeric protein, induced scattering of PECs associated with internalization of Endo180 into endosomes, loss of E-cadherin (CDH1/ECAD), and unzipping of cell-cell junctions. These findings are the first to demonstrate that a CTLD acts as a suppressor and regulatory switch for EMT; thus, positing that stabilization of Endo180-CD147 complex is a viable therapeutic strategy to improve rates of prostate cancer survival.Implications: This study identifies the interaction between CTLD4 in Endo180 and CD147 as an EMT suppressor and indicates that stabilization of this molecular complex improves prostate cancer survival rates.

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Section: Discussionmentioning

confidence: 99%

Survival Outcome and EMT Suppression Mediated by a Lectin Domain Interaction of Endo180 and CD147

Rodriguez-Teja

Gronau

Minamidate

et al. 2015

Molecular Cancer Research

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“…The disease is characterized by evolution from a clinically localized hormone-naïve state to an eventually castrateresistant metastatic state (1). The widespread use of screening serum prostate-specific antigen (PSA) has resulted in downward stage migration and increased diagnosis of localized low-grade prostate cancers, leading to overdiagnosis and overtreatment (2).…”

mentioning

confidence: 99%

Molecular Imaging of Prostate Cancer with PET

Jadvar¹

2013

J Nucl Med

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Molecular imaging is paving the way for precision and personalized medicine. In view of the significant biologic and clinical heterogeneity of prostate cancer, molecular imaging is expected to play an important role in the evaluation of this prevalent disease. The natural history of prostate cancer spans from an indolent localized process to biochemical relapse after radical treatment with curative intent to a lethal castrate-resistant metastatic disease. The ongoing unraveling of the complex tumor biology of prostate cancer uniquely positions molecular imaging with PET to contribute significantly to every clinical phase of prostate cancer evaluation. The purpose of this article was to provide a concise review of the current state of affairs and potential future developments in the diagnostic utility of PET in prostate cancer.

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“…In prostate cancer cells, androgen-regulated transcription factors, including Forkhead Box A1, GATA-binding protein 2 and Octamer-binding protein 1, are recruited to AR chromosome binding sites (15,16). In coordination with AR, the AR-regulated signaling pathway is activated to modulate the overexpression of PSA, transmembrane protease serine 2 (TMPRSS2) and other genes.…”

Section: Prostate Cancer Genomics and Molecular Subtypesmentioning

confidence: 99%

“…In coordination with AR, the AR-regulated signaling pathway is activated to modulate the overexpression of PSA, transmembrane protease serine 2 (TMPRSS2) and other genes. TMPRSS2, a transmembrane serine protease, is expressed specifically in the prostate gland (15,16). ETS transcription factors are important regulators of cell proliferation, differentiation and apoptosis (17).…”

Section: Prostate Cancer Genomics and Molecular Subtypesmentioning

confidence: 99%

“…ETS transcription factors are important regulators of cell proliferation, differentiation and apoptosis (17). Androgen-regulated ETS gene fusions are the most commonly identified genetic alterations and are present in >50% of primary and metastatic prostate cancer cases (15,18). Among the established gene fusions, transcriptional regulator Erg (ERG)-TMPRSS2 is frequently identified.…”

Section: Prostate Cancer Genomics and Molecular Subtypesmentioning

confidence: 99%

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The context of prostate cancer genomics in personalized medicine

Liu

2017

Oncology Letters

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Abstract. Prostate cancer is one of the most common types of cancer in males. Heterogeneous genomic aberrations may lead to prostate cancer onset, progression and metastasis. This heterogeneity also contributes to the variety in cancer risk and outcomes, different drug responses and progression, observed between individual patients. Classical prognostic factors, including prostate-specific antigen, Gleason Score and clinical tumor staging, are not sufficient to portray the complexity of a clinically relevant cancer diagnosis, risk prognosis, treatment choice and therapy monitoring. There is a requirement for novel genetic biomarkers in order to understand the oncogenic heterogeneity in a patient-personalized clinical setting and to improve the efficacy of risk prognosis and treatment choice. A number of biomarkers and gene panels have been established from patient sample cohort studies. These previous studies have provided distinct information to the investigation of heterogeneous malignancy in prostate cancer, which aids in clinical decision-making. Biomarker-guided therapies may facilitate the effective selection of drugs during early treatment; therefore, are beneficial to the individual patient. A non-invasive approach allows for convenient and repeated sampling to screen for cancer and monitor treatment response without the requirement for invasive tissue biopsies. With the current availability of numerous advanced technologies, reliable detection of the minimal tumor residues present following treatment may become clinical practice and, therefore, inform further in the field of personalized medicine.

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Molecular Pathogenesis and Progression of Prostate Cancer

Cited by 99 publications

References 138 publications

Survival Outcome and EMT Suppression Mediated by a Lectin Domain Interaction of Endo180 and CD147

Survival Outcome and EMT Suppression Mediated by a Lectin Domain Interaction of Endo180 and CD147

Molecular Imaging of Prostate Cancer with PET

The context of prostate cancer genomics in personalized medicine

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