MicroRNA expressions associated with progression of prostate cancer cells to antiandrogen therapy resistance

Ottman, Richard; Nguyen, Camha; Lorch, Robert; Chakrabarti, Ratna

doi:10.1186/1476-4598-13-1

Cited by 187 publications

(162 citation statements)

References 139 publications

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“…Especially germane to contemplating new targeting strategies are the key observations from several studies demonstrating a clear association of VM tumor cells expressing several stem cell markers cited above in addition to CD133 concomitant with ABCB5 drug resistance protein (Frank et al, 2011; Lai et al, 2012; Zhang et al, 2014; Lezcano et al, 2014;). Furthermore, emerging evidence indicates that conventional therapies are not effectively targeting these stem cell subpopulations, rather they are leading to their enhanced selection and growth resulting in rampant tumor progression (Hardy et al, 2015).…”

Section: Key Signaling Pathways In Vascular Mimicrymentioning

confidence: 99%

Tumor cell vascular mimicry: Novel targeting opportunity in melanoma

Hendrix

Seftor

et al. 2016

Pharmacology & Therapeutics

133

136

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In 1999, the American Journal of Pathology published an article, entitled “Vascular channel formation by human melanoma cells in vivo and in vitro: vasculogenic mimicry” by Maniotis and colleagues, which ignited a spirited debate for several years and earned the journal's distinction of a “citation classic” (Maniotis et al., 1999). Tumor cell vasculogenic mimicry (VM), also known as vascular mimicry, describes the plasticity of aggressive cancer cells forming de novo vascular networks and is associated with the malignant phenotype and poor clinical outcome. The tumor cells capable of VM share the commonality of a stem cell-like, transendothelial phenotype, which may be induced by hypoxia. Since its introduction as a novel paradigm for melanoma tumor perfusion, many studies have contributed new findings illuminating the underlying molecular pathways supporting VM in a variety of tumors, including carcinomas, sarcomas, glioblastomas, astrocytomas, and melanomas. Of special significance is the lack of effectiveness of angiogenesis inhibitors on tumor cell VM, suggesting a selective resistance by this phenotype to conventional therapy. Facilitating the functional plasticity of tumor cell VM are key proteins associated with vascular, stem cell, extracellular matrix, and hypoxia-related signaling pathways -- each deserving serious consideration as potential therapeutic targets and diagnostic indicators of the aggressive, metastatic phenotype. This review highlights seminal findings pertinent to VM, including the effects of a novel, small molecular compound, CVM-1118, currently under clinical development to target VM, and illuminates important molecular pathways involved in the suppression of this plastic, aggressive phenotype, using melanoma as a model.

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Section: Key Signaling Pathways In Vascular Mimicrymentioning

confidence: 99%

Tumor cell vascular mimicry: Novel targeting opportunity in melanoma

Hendrix

Seftor

et al. 2016

Pharmacology & Therapeutics

133

136

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“…Loss of the tumor-suppressive miR-221/222 cluster enhanced migration and invasion in PCa cells targeting Ecm29, whose precise mechanisms in cancer cells remain unknown but it is involved in cancer cells invasion. Ottman et al [69], comparing androgen sensitive and resistant PCa cell lines, identified 43 miRNAs that are significantly altered during progression of PCa cells to treatment resistance, suggesting their involvement in the development of CRPC. Specific changes in miRNA expression in CRPC patients could be used as a new predictive tool for monitoring the susceptibility of development of CRPC.…”

Section: Role Of Mirnas In Prostate Cancermentioning

confidence: 99%

miRNAs as novel biomarkers in the management of prostate cancer

Filella

Foj

2017

Clinical Chemistry and Laboratory Medicine (CCLM)

100

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microRNAs (miRNAs) are small non-coding RNAs that control gene expression posttranscriptionally and are part of the giant non codifying genoma. Cumulating data suggest that miRNAs are promising potential biomarkers for many diseases, including cancer. Prostate cancer (PCa) detection is currently based in the serum prostate-specific antigen biomarker and digital rectal examination. However, these methods are limited by a low predictive value and the adverse consequences associated with overdiagnosis and overtreatment. New biomarkers that could be used for PCa detection and prognosis are still needed. Recent studies have demonstrated that aberrant expressions of microRNAs are associated with the underlying mechanisms of PCa. This review attempts to extensively summarize the current knowledge of miRNA expression patterns, as well as their targets and involvement in PCa pathogenesis. We focused our review in the value of circulating and urine miRNAs as biomarkers in PCa patients, highlighting the existing discrepancies between different studies, probably associated with the important methodological issues related to their quantitation and normalization. The majority of studies have been performed in serum or plasma, but urine obtained after prostate massage appears as a new way to explore the usefulness of miRNAs. Large screening studies to select a miRNA profile have been completed, but bioinformatics tools appear as a new approach to select miRNAs that are relevant in PCa development.Promising preliminary results were published concerning miR-141, miR-375 and miR-21, but larger and prospective studies using standardized methodology are necessary to define the value of miRNAs in the detection and prognosis of PCa.

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“…Recently, it has been observed that altered expression of miRNAs is associated with progression of androgen sensitive prostate cells to antiandrogen therapy resistance (56). Moreover, some studies described the involvement of AR signaling in the regulation of specific miRNAs in PCa (6,57).…”

Section: Discussionmentioning

confidence: 99%

miR-22 and miR-29a Are Members of the Androgen Receptor Cistrome Modulating LAMC1 and Mcl-1 in Prostate Cancer

Pasqualini

Puhr

et al. 2015

Molecular Endocrinology

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The normal prostate as well as early stages and advanced prostate cancer (PCa) require a functional androgen receptor (AR) for growth and survival. The recent discovery of microRNAs (miRNAs) as novel effector molecules of AR disclosed the existence of an intricate network between AR, miRNAs and downstream target genes. In this study DUCaP cells, characterized by high content of wild-type AR and robust AR transcriptional activity, were chosen as the main experimental model. By integrative analysis of chromatin immunoprecipitation-sequencing (ChIP-seq) and microarray expression profiling data, miRNAs putatively bound and significantly regulated by AR were identified. A direct AR regulation of miR-22, miR-29a, and miR-17-92 cluster along with their host genes was confirmed. Interestingly, endogenous levels of miR-22 and miR-29a were found to be reduced in PCa cells expressing AR. In primary tumor samples, miR-22 and miR-29a were less abundant in the cancerous tissue compared with the benign counterpart. This specific expression pattern was associated with a differential DNA methylation of the genomic AR binding sites. The identification of laminin gamma 1 (LAMC1) and myeloid cell leukemia 1 (MCL1) as direct targets of miR-22 and miR-29a, respectively, suggested a tumor-suppressive role of these miRNAs. Indeed, transfection of miRNA mimics in PCa cells induced apoptosis and diminished cell migration and viability. Collectively, these data provide additional information regarding the complex regulatory machinery that guides miRNAs activity in PCa, highlighting an important contribution of miRNAs in the AR signaling.

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MicroRNA expressions associated with progression of prostate cancer cells to antiandrogen therapy resistance

Cited by 187 publications

References 139 publications

Tumor cell vascular mimicry: Novel targeting opportunity in melanoma

Tumor cell vascular mimicry: Novel targeting opportunity in melanoma

miRNAs as novel biomarkers in the management of prostate cancer

miR-22 and miR-29a Are Members of the Androgen Receptor Cistrome Modulating LAMC1 and Mcl-1 in Prostate Cancer

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