miR-205 in Breast Cancer: State of the Art

Plantamura, Ilaria; Cataldo, Alessandra; Cosentino, Giulia; Iorio, Marilena V.

doi:10.3390/ijms22010027

Cited by 47 publications

(26 citation statements)

References 71 publications

(80 reference statements)

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“…MaSCs are also characterized by the high expression of miR-205 and miR-22 and by the downregulation of let-7 and miR-93 [289]. MiR-205 is aberrantly expressed in breast cancer tissues, and a decrease in its expression correlates with the aggressiveness of the breast cancer phenotype; therefore, its downregulation is associated with poor prognosis and can be used as tumor biomarker [290]. Studies conducted in conditional mammary gland-specific transgenic mouse models revealed that miR-22 promotes the expansion of the stem-cell compartment, inducing tumor development and aggressive metastatic disease [291].…”

Section: Mirnas Expressed In Mascs and Breast Cscsmentioning

confidence: 99%

MicroRNAs and Stem-like Properties: The Complex Regulation Underlying Stemness Maintenance and Cancer Development

et al. 2021

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Embryonic stem cells (ESCs) have the extraordinary properties to indefinitely proliferate and self-renew in culture to produce different cell progeny through differentiation. This latter process recapitulates embryonic development and requires rounds of the epithelial–mesenchymal transition (EMT). EMT is characterized by the loss of the epithelial features and the acquisition of the typical phenotype of the mesenchymal cells. In pathological conditions, EMT can confer stemness or stem-like phenotypes, playing a role in the tumorigenic process. Cancer stem cells (CSCs) represent a subpopulation, found in the tumor tissues, with stem-like properties such as uncontrolled proliferation, self-renewal, and ability to differentiate into different cell types. ESCs and CSCs share numerous features (pluripotency, self-renewal, expression of stemness genes, and acquisition of epithelial–mesenchymal features), and most of them are under the control of microRNAs (miRNAs). These small molecules have relevant roles during both embryogenesis and cancer development. The aim of this review was to recapitulate molecular mechanisms shared by ESCs and CSCs, with a special focus on the recently identified classes of microRNAs (noncanonical miRNAs, mirtrons, isomiRs, and competitive endogenous miRNAs) and their complex functions during embryogenesis and cancer development.

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Section: Mirnas Expressed In Mascs and Breast Cscsmentioning

confidence: 99%

MicroRNAs and Stem-like Properties: The Complex Regulation Underlying Stemness Maintenance and Cancer Development

et al. 2021

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“…miR-205 has been detected in serum of BC patients with a decreasing expression from the less aggressive BC subtypes to the more aggressive ones, mainly in HER2-positive and triple-negative tumors [ 44 , 45 ]. It targets HER3 directly, inhibiting SKBr3 in BC cell lines [ 46 , 47 ].…”

Section: Mirnas In Her2-positive Breast Cancermentioning

confidence: 99%

“…It targets HER3 directly, inhibiting SKBr3 in BC cell lines [ 46 , 47 ]. Its oncosuppressive role is also linked by EMT suppression [ 45 ].…”

Section: Mirnas In Her2-positive Breast Cancermentioning

confidence: 99%

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Circulating and Intracellular miRNAs as Prognostic and Predictive Factors in HER2-Positive Early Breast Cancer Treated with Neoadjuvant Chemotherapy: A Review of the Literature

Isca

Piacentini

Mastrolia

et al. 2021

Cancers

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MicroRNAs (miRNA) are small noncoding RNAs that can act as both oncogene and tumor suppressors. Deregulated miRNA expression has been detected in human cancers, including breast cancer (BC). Considering their important roles in tumorigenesis, miRNAs have been investigated as potential prognostic and diagnostic biomarkers. Neoadjuvant setting is an optimal model to investigate in vivo the mechanism of treatment resistance. In the management of human epidermal growth factor receptor-2 (HER2)-positive early BC, the anti-HER2-targeted therapies have drastically changed the survival outcomes. Despite this, growing drug resistance due to the pressure of therapy is relatively frequent. In the present review, we focused on the main miRNAs involved in HER2-positive BC tumorigenesis and discussed the recent evidence on their predictive and prognostic value.

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“…Oxidative stress resulted in alterations in protein function and oxidation of mitochondrial DNA. At the same time, mitochondrial damage induced the generation of ROS [ 23 ]. Ultimately, oxidative stress activates caspases and promotes cell apoptosis [ 24 ].…”

Section: Introductionmentioning

confidence: 99%

Inhibiting miR‐205 Alleviates Cardiac Ischemia/Reperfusion Injury by Regulating Oxidative Stress, Mitochondrial Function, and Apoptosis

Zeng

et al. 2021

Oxidative Medicine and Cellular Longevity

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Background. miR-205 is important for oxidative stress, mitochondrial dysfunction, and apoptosis. The roles of miR-205 in cardiac ischemia/reperfusion (I/R) injury remain unknown. The aim of this research is to reveal whether miR-205 could regulate cardiac I/R injury by focusing upon the oxidative stress, mitochondrial function, and apoptosis. Methods. Levels of miR-205 and Rnd3 were examined in the hearts with I/R injury. Myocardial infarct size, cardiac function, oxidative stress, mitochondria function, and cardiomyocyte apoptosis were detected in mice with myocardial ischemia/reperfusion (MI/R) injury. The primary neonatal cardiomyocytes underwent hypoxia/reoxygenation (H/R) to simulate MI/R injury. Results. miR-205 levels were significantly elevated in cardiac tissues from I/R in comparison with those from Sham. In comparison with controls, levels of Rnd3 were significantly decreased in the hearts from mice with MI/R injury. Furthermore, inhibiting miR-205 alleviated MI/R-induced apoptosis, reduced infarct size, prevented oxidative stress increase and mitochondrial fragmentation, and improved mitochondrial functional capacity and cardiac function. Consistently, overexpression of miR-205 increased infarct size and promoted apoptosis, oxidative stress, and mitochondrial dysfunction in mice with MI/R injury. In cultured mouse neonatal cardiomyocytes, downregulation of miR-205 reduced oxidative stress in H/R-treated cardiomyocytes. Finally, inhibiting Rnd3 ablated the cardioprotective effects of miR-205 inhibitor in MI/R injury. Conclusions. We conclude that inhibiting miR-205 reduces infarct size, improves cardiac function, and suppresses oxidative stress, mitochondrial dysfunction, and apoptosis by promoting Rnd3 in MI/R injury. miR-205 inhibitor-induced Rnd3 activation is a valid target to treat MI/R injury.

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miR-205 in Breast Cancer: State of the Art

Cited by 47 publications

References 71 publications

MicroRNAs and Stem-like Properties: The Complex Regulation Underlying Stemness Maintenance and Cancer Development

MicroRNAs and Stem-like Properties: The Complex Regulation Underlying Stemness Maintenance and Cancer Development

Circulating and Intracellular miRNAs as Prognostic and Predictive Factors in HER2-Positive Early Breast Cancer Treated with Neoadjuvant Chemotherapy: A Review of the Literature

Inhibiting miR‐205 Alleviates Cardiac Ischemia/Reperfusion Injury by Regulating Oxidative Stress, Mitochondrial Function, and Apoptosis

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