Control of tumor and microenvironment cross-talk by miR-15a and miR-16 in prostate cancer

Musumeci, Maria; Coppola, Valeria; Addario, Antonio; Patrizii, Michele; Maugeri‐Saccà, Marcello; Memeo, Lorenzo; Colarossi, Cristina; Francescangeli, Federica; Biffoni, Mauro; Collura, Devis; Giacobbe, Alessandro; D’Urso, Leonardo; Falchi, Mario; Venneri, Mary Anna; Muto, Giovanni; Maria, Ruggero De; Bonci, Desirée

doi:10.1038/onc.2011.140

Cited by 220 publications

(174 citation statements)

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“…These data may help to develop new therapeutic strategies to target the prostate tumor stroma under androgen-manipulated conditions. Interestingly, a recent study has demonstrated that downregulation of the micro-RNAs miR-15 and miR-16 in prostate cancer-associated fibroblasts (CAFs) promotes tumor growth and progression through the reduced post-transcriptional repression of FGF2 and of its receptor FGFR1 [90]. Moreover, reconstitution of miR-15 and miR-16 significantly impaired the tumor-supportive capability of stromal cells in vitro and in vivo, thus enforcing the therapeutic concept aimed at reconstituting the expression of these micro-RNAs in advanced prostate cancer [90].…”

Section: The Role Of the Fgf/fgfr System In Tumor/stroma Cross-talkmentioning

confidence: 99%

Blocking the FGF/FGFR system as a ⿿two-compartment⿿ antiangiogenic/antitumor approach in cancer therapy

Giacomini

Chiodelli

Matarazzo

et al. 2016

Pharmacological Research

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a b s t r a c tFibroblast growth factors (FGFs) are a family of pleiotropic factors produced by stromal and parenchymal tumor cells. Even though FGFs have been firstly characterized as angiogenic factors, they exert autocrine and paracrine functions not only on endothelial cells but also on tumor cells and other stromal components. Thus, the FGF/FGF receptor (FGFR) pathway may represent a key player in tumor growth by regulating the complex cross-talk between stromal and tumor compartments.The ligand dependent or independent activation of the FGF/FGFR system by gene upregulation, oncogenic mutation or amplification occurs in a variety of human tumors and is implicated in various key steps of tumor growth and progression. In addition, FGF/FGFR activation has been described as a mechanism of tumor escape in response to antiangiogenic/anti-VEGF therapies.Experimental and clinical evidences provide a compelling biologic rationale for the development of anti-FGF/FGFR targeting agents in cancer therapy. However, the development of drugs specifically targeting the FGF/FGFR pathway proved to be difficult, also due to the high redundancy and pleiotropic effects of FGF and FGFR family members. On the other hand, the possibility to develop "two-compartment" targeting agents endowed with both antiangiogenic and antitumor activities remains promising.Here we will review the preclinical and clinical approaches and potential therapeutics currently available to block the FGF/FGFR system in human cancer.

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Section: The Role Of the Fgf/fgfr System In Tumor/stroma Cross-talkmentioning

confidence: 99%

Blocking the FGF/FGFR system as a ⿿two-compartment⿿ antiangiogenic/antitumor approach in cancer therapy

Giacomini

Chiodelli

Matarazzo

et al. 2016

Pharmacological Research

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show abstract

“…There are some miRNAs that have been found to influence tumor microenvironment. 24 This extensive body of knowledge points to miRNAs as potentially being novel cancer biomarkers, and as such they have several advantageous features. The small size and distinctive biochemical structure of miRNAs makes them resistant to endogenous RNase activity.…”

Section: Mirnas As Biomarkers In Prostate Cancer Pathogenesismentioning

confidence: 99%

MicroRNAs in prostate cancer: from biomarkers to molecularly-based therapeutics

Gordanpour

Nam

Sugar

et al. 2012

Prostate Cancer Prostatic Dis

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MicroRNAs (miRNAs) are effective regulators of gene expression that have a significant role in the pathogenesis of prostate and various other cancers. The high prevalence of aberrant miRNA expression in prostate cancer, and miRNAs' distinctive properties, give much hope that they can be used as biomarkers and next generation of molecular anticancer therapeutics. Herein, we review the literature on miRNA involvement in prostate cancer pathogenesis and the current understanding of their role as oncogenes, tumor suppressors and metastasis-regulators. We also review the latest research on miRNAs in prostate cancer preclinical studies and clinical trials, and highlight the advantages and challenges of possible miRNA-based therapies. The emerging information regarding the biology of miRNAs in prostate cancer is promising, and may lead to a role(s) for these molecules as diagnostic/prognostic markers and effective therapeutic tools for better molecularly targeted treatment of prostate cancer.

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“…Lately miRNA has also become implicated in signaling between stromal and epithelial cells and some recent reports [28,29] have provided evidence suggesting that traffic of miRNA subtypes between disseminated cancer cells and bone marrow stromal cells can influence whether the cancer cells establish metastatic colonies or remain in dormant state. If these findings are corroborated, it will show that non-proteinaceous molecules also convey signals between interacting cell populations in the tumor microenvironment, which can determine whether tumor cells can fulfill an already activated, intrinsic potential towards malignant behavior.…”

Section: Ii) Cancer Formation: Microscopic and Cellular Aspectsmentioning

confidence: 99%

Clinical and Biological Implications of the Tumor Microenvironment

Tarin¹

2012

Cancer Microenvironment

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In normal tissues and organs, the activities of the constituent cells are strictly restricted to the tasks assigned to them during development. In addition they (with the exception of leukocytes) remain inflexibly confined to their territorial domains by regulatory interactions with their neighbors. This creates specialized local micro-environments in which structure and function are orderly, stable and tightly controlled by feed-back loops, within interacting regulatory networks. This system has considerable ability to adapt to changing conditions. In contrast, the microenvironment in regions where tumors are forming and expanding is characterized by progressive loss of specialized or differentiated cellular functions, disorderly molecular signals, degeneration of microscopical organ structure. This, coupled with the traffic of cells into and out of the tumor, often culminating in local invasion and metastasis to other organs. The nature of these disturbed molecular and cellular interactions is, by definition, highly unstable and increasingly unpredictable as time passes. It also varies between different tumors, sometimes even leading to regression. However, systematic analysis of this dysfunction in the tumor microcosm, using multiple modern research techniques, has revealed that all actively growing primary and secondary neoplasms share an absolute dependency upon support from adjacent non-neoplastic cells of the host. This support, in turn, continuously depends upon dynamic interplay between tumor and host cell populations, via signaling molecules and surface receptors in the tumor microenvironment. Such interplay determines the fate of the growing neoplasm. Such information, described and evaluated in this article, provides important new insights into the etiology of carcinogenesis and how tumor growth, invasion and metastasis might be therapeutically arrested. The facts and concepts assembled below, regarding the cancer microenvironment, demonstrate how modern molecular findings reveal the impact of the wide range of cancer diseases upon the internal cellular, tissue and organ environments of the whole individual and how this applies to designing new work to improve human cancer diagnosis and treatment. The article discusses several specific types of experimentally-induced and clinically common cancers to derive principles useful for interpreting events in the tumor microenvironment, which apply to cancers in general and especially to human malignant disease.

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Control of tumor and microenvironment cross-talk by miR-15a and miR-16 in prostate cancer

Cited by 220 publications

References 50 publications

Blocking the FGF/FGFR system as a ⿿two-compartment⿿ antiangiogenic/antitumor approach in cancer therapy

Blocking the FGF/FGFR system as a ⿿two-compartment⿿ antiangiogenic/antitumor approach in cancer therapy

MicroRNAs in prostate cancer: from biomarkers to molecularly-based therapeutics

Clinical and Biological Implications of the Tumor Microenvironment

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