miR-210 as a marker of chronic hypoxia, but not a therapeutic target in prostate cancer

Quéro, L.; Dubois, Ludwig; Lieuwes, Natasja G.; Hennequin, Christophe

doi:10.1016/j.radonc.2011.05.063

Cited by 41 publications

(35 citation statements)

References 34 publications

(45 reference statements)

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“…The high levels of miR-210 are also identified in lymphoma and lung cancer patients [166–168]. It has been documented that hypoxia highly induces the miR-210 expression in all the cells tested including cancer cells [169–178], suggesting a close relationship of miR-210 with hypoxia-mediated ROS production. However, the role of ROS-mediated miR-210 in tumorigenesis is still not characterized and understood.…”

Section: The Role Of Mirnas In the Regulation Of Ros Productionmentioning

confidence: 99%

“…However, the role of ROS-mediated miR-210 in tumorigenesis is still not characterized and understood. The hypoxia-induced expression of miR-210 is known to promote the expression of hypoxia responsive targets VEGF and CAIX in human pancreatic cancer cells by a HIF-1α-dependent mechanism [171, 178], which clearly suggests a regulatory role of miR-210 in tumor angiogenesis [108, 176, 179–182], resulting in tumor aggressive phonotypes. Hypoxia-induced expression of miR-210 has been found to participate in the modulation of DNA damage repair pathway.…”

Section: The Role Of Mirnas In the Regulation Of Ros Productionmentioning

confidence: 99%

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Targeting CSCs in Tumor Microenvironment: The Potential Role of ROS-Associated miRNAs in Tumor Aggressiveness

Bao¹,

Azmi²,

Li³

et al. 2013

CSCR

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Reactive oxygen species (ROS) have been widely considered as critical cellular signaling molecules involving in various biological processes such as cell growth, differentiation, proliferation, apoptosis, and angiogenesis. The homeostasis of ROS is critical to maintain normal biological processes. Increased production of ROS, namely oxidative stress, due to either endogenous or exogenous sources causes irreversible damage of bio-molecules such as DNA, proteins, lipids, and sugars, leading to genomic instability, genetic mutation, and altered gene expression, eventually contributing to tumorigenesis. A great amount of experimental studies in vitro and in vivo have produced solid evidence supporting that oxidative stress is strongly associated with increased tumor cell growth, treatment resistance, and metastasis, and all of which contribute to tumor aggressiveness. More recently, the data have indicated that altered production of ROS is also associated with cancer stem cells (CSCs), epithelial-to-mesenchymal transition (EMT), and hypoxia, the most common features or phenomena in tumorigenesis and tumor progression. However, the exact mechanism by which ROS is involved in the regulation of CSC and EMT characteristics as well as hypoxia- and, especially, HIF-mediated pathways is not well known. Emerging evidence suggests the role of miRNAs in tumorigenesis and progression of human tumors. Recently, the data have indicated that altered productions of ROS are associated with deregulated expression of miRNAs, suggesting their potential roles in the regulation of ROS production. Therefore, targeting ROS mediated through the deregulation of miRNAs by novel approaches or by naturally occurring anti-oxidant agents such as genistein could provide a new therapeutic approach for the prevention and/or treatment of human malignancies. In this article, we will discuss the potential role of miRNAs in the regulation of ROS production during tumorigenesis. Finally, we will discuss the role of genistein, as a potent anti-tumor agent in the regulation of ROS production during tumorigenesis and tumor development.

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Section: The Role Of Mirnas In the Regulation Of Ros Productionmentioning

confidence: 99%

Section: The Role Of Mirnas In the Regulation Of Ros Productionmentioning

confidence: 99%

Targeting CSCs in Tumor Microenvironment: The Potential Role of ROS-Associated miRNAs in Tumor Aggressiveness

Bao¹,

Azmi²,

Li³

et al. 2013

CSCR

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“…Reduced survival of cells devoid of miR-210 in normoxia and/or hypoxia is well documented (7)(8)(9)(13)(14)(15)(16). Moreover, miR-210 plays an instrumental role in the cytoprotection afforded to bone marrow-derived mesenchymal stem cells by ischemia/reoxygenation, supporting their survival under subsequently longer exposure to anoxia and following engraftment in the infarcted heart (17).…”

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confidence: 99%

Hypoxia-inducible Factor 1-α Induces miR-210 in Normoxic Differentiating Myoblasts

Cicchillitti

Stefano

Isaia

et al. 2012

Journal of Biological Chemistry

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Background: miR-210 hypoxamir is induced by Hif1a in hypoxic cells. Results: miR-210 expression increased during myogenic differentiation in normoxia with a Hif1a-dependent mechanism. Moreover, miR-210 displayed a cytoprotective role in response to mitochondrial dysfunction and oxidative stress. Conclusion: miR-210 regulation and function extend beyond cell response to hypoxia. Significance: Identifying miR-210 as a potential target in skeletal muscle disorders.

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“…Combining anti-miR-210 treatment and existing therapies (chemotherapy and radiotherapy) is a plausible approach due to the inherent resistance of hypoxic cells to these treatments. Yet, only one in vitro prostate cancer study has been published, but disappointingly without signs of effect of a miR-210 inhibitor when combined with radiotherapy43.…”

Section: Discussionmentioning

confidence: 99%

Fibroblast miR-210 overexpression is independently associated with clinical failure in Prostate Cancer – a multicenter (in situ hybridization) study

Andersen

Richardsen

Moi

et al. 2016

Sci Rep

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There is a need for better prognostication in prostate cancer (PC). “The micromanager of hypoxia”, microRNA-210 (miR-210) is directly linked to hypoxia, is overexpressed in PC and has been implied in tumor cell-fibroblast crosstalk. We investigated the prognostic impact of miR-210 in tumor cells and fibroblasts in PC. Tumor and stromal samples from a multicenter PC cohort of 535 prostatectomy patients were inserted into tissue microarrays. To investigate the expression of miR-210, we used in situ hybridization and two pathologists semiquantitatively scored its expression. Overexpression of miR-210 in tumor cells was not associated to biochemical failure-free survival (BFFS, p = 0.85) or clinical failure-free survival (CFFS, p = 0.09). However, overexpression of miR-210 in fibroblasts was significantly associated to a poor CFFS (p = 0.001), but not BFFS (p = 0.232). This feature was validated in both cohorts. Overexpression of miR-210 was independently associated with a reduced CFFS (HR = 2.76, CI 95% 1.25–6.09, p = 0.012). Overexpression of miR-210 in fibroblasts is independently associated with a poor CFFS. This highlights the importance of fibroblasts and cellular compartment crosstalk in PC. miR-210 is a candidate prognostic marker and potential therapeutic target in PC.

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miR-210 as a marker of chronic hypoxia, but not a therapeutic target in prostate cancer

Abstract: miR-210 could be an interesting marker of chronic hypoxia irrespective of the androgen dependency and should, therefore, be tested as a prognostic marker in high risk prostate cancer patients.

Cited by 41 publications

References 34 publications

Targeting CSCs in Tumor Microenvironment: The Potential Role of ROS-Associated miRNAs in Tumor Aggressiveness

Targeting CSCs in Tumor Microenvironment: The Potential Role of ROS-Associated miRNAs in Tumor Aggressiveness

Hypoxia-inducible Factor 1-α Induces miR-210 in Normoxic Differentiating Myoblasts

Fibroblast miR-210 overexpression is independently associated with clinical failure in Prostate Cancer – a multicenter (in situ hybridization) study

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