The Oncogenic Role of miR-155 in Breast Cancer

Mattiske, Sam; Suetani, Rachel J.; Neilsen, Paul M.; Callen, David F.

doi:10.1158/1055-9965.epi-12-0173

Cited by 253 publications

(176 citation statements)

References 88 publications

(92 reference statements)

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“…[6][7][8][9] Sustained proliferation is a hallmark of transformed cells. Knockdown of BIC in malignant MyLa2059 cells entailed a 40% decrease of miR-155 expression (Fig.…”

Section: Resultsmentioning

confidence: 99%

“…It has been found overexpressed in hematological 4,5 as well as a number of solid cancers. [6][7][8][9] miR-155 is localized within an exon of its precursor gene BIC (B cell integration cluster or pri-miR-155). 4 Transiently elevated expression of miR-155 plays a role in the activation of several types of immune cells, 2,[10][11][12] whereas constitutively high levels of this miRNA can result in the development of malignancies by increase of genomic instability 13,14 and sustained proliferation and survival 5,15 of malignant cells.…”

Section: Introductionmentioning

confidence: 99%

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STAT5-mediated expression of oncogenic miR-155 in cutaneous T-cell lymphoma

et al. 2013

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“…[6][7][8][9] Sustained proliferation is a hallmark of transformed cells. Knockdown of BIC in malignant MyLa2059 cells entailed a 40% decrease of miR-155 expression (Fig.…”

Section: Resultsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

STAT5-mediated expression of oncogenic miR-155 in cutaneous T-cell lymphoma

et al. 2013

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“…The miR155 also has opposite actions, it can be oncogenic (the targets are BCL2, FOXO3a, RhoA) or tumor suppressor (the targets are TGF-beta/SMAD) [158]. The literature about miR155 is vast, and we suggest the articles by Higgs and Slack [158] and Mattiske et al [159] for a deep reading. Besides these two miRNAs cited above, others miRNAs are upregulated by ROS, such as miR23, miR200, miR210, etc., affecting migration, invasion; tumor growth, angiogenesis; cell cycle, DNA damage (among others), respectively [126].…”

Section: Some Ros Such As Omentioning

confidence: 97%

Oxidative Stress: Noxious but Also Vital

Bagatini¹,

Jaques²,

Oliveira³

et al. 2018

Novel Prospects in Oxidative and Nitrosative Stress

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The imbalance between reactive oxygen species (ROS) production and antioxidant defenses determines the condition called oxidative stress. When there is an increase in ROS production or a decrease in the antioxidant defenses, this systemic antioxidant/pro-oxidant imbalance may lead to the accumulation of oxidative damage, which, in turn, may lead to a modification of biomolecules. These consist of reactions resulting in protein adducts, DNA oxidation, and formation of lipid peroxides, which, in turn, reduce the cellular functional capacity and increase the risk of disease development. The body has natural scavenging systems against free radicals and other reactive species. However, sometimes the endogenous antioxidant capacity is exceeded by the production of ROS. When this occurs, exogenous antioxidants exert important function for the human health. These bioactive compounds act preventing and neutralizing the formation of new reactive species and free radical s .I ns o m ec a s e s ,a n increase of ROS can help the host to resolve an infection or even to control the tumor growth. Finally, the levels of ROS can be perceived by signal transduction pathways involving known targets(i.e.,p53,Ras,andNF-κB) and regulate physiopathological events such as the cellular cycle, apoptosis, and inflammation.Keywords: reactive species, cellular oxidation, antioxidant system, health, disease © 2018 The Author(s). Licensee IntechOpen. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Cellular respiration and generation of reactive species in the mitochondria: implications in cell viability and agingOxidative phosphorylation is the center of energy metabolism in plants, animals and several microbial life forms [1]. In eukaryotes, this process occurs in mitochondria. The mitochondria is a cytoplasmic organelle surrounded by two membranes, outer and inner membrane, which main function is the production of most of the phosphate compounds necessary for the energetic balance of the cell. In addition, other functions such as the regulation of the body'sheatgeneration [2][3][4] programmed cell death [5][6][7], reactive oxygen species (ROS) generation and cell signaling [8] is also associated with mitochondria. Cellular vitality is directly related to mitochondria, and mitochondrial dysfunctions are frequent causes of accidental cell death [5,[9][10][11], cancer [12, 13], diabetes [14][15][16] and neurodegenerative diseases [17][18][19], among others.The characterization of the respiratory electron chain could be performed in studies using the fractionation of its components by certain detergents that at low concentrations break the interactions between proteins and lipids in the membranes, leaving associations between proteins intact [20]. In electron transport chain, through this process, four protein complexes were found....

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“…Other targets of miR-21 includes PTEN in hepatocellular carcinoma (49); tumor suppressor genes ANP32A (nuclear phosphoprotein 32 family, member A/alias pp32/ LANP) in human prostate carcinoma cells, and SMARCA4 (alias BRG1) in B-cell lymphoma (50); maspin, a tumor suppressor in invasion and metastasis (51), and tropomyosin 1 (TPM1) in breast cancer MCF-7 cells (52). Another miRNA acting as an oncogene is miR-155 whose role in breast cancer progression has been studied recently (53). It is highly upregulated in breast cancer where it targets tumor suppressor gene SOCS1 (54).…”

Section: Oncomirsmentioning

confidence: 99%

Genomic and Epigenomic Cross-talks in the Regulatory Landscape of miRNAs in Breast Cancer

Samantarrai

Dash

Chhetri

et al. 2013

Molecular Cancer Research

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MicroRNAs (miRNA) are a class of endogenous, small noncoding RNAs found in animals, plants, and viruses that control their target gene expression posttranscriptionally. They are involved in a wide array of biological processes including cell differentiation, development, cell death and homeostasis, and fine-tune the regulation of these pathways. Their aberrant expressions have been associated with different diseases. These small RNAs are also known to function as oncogenes, oncosupressor genes, modulators of metastatic spread, and regulators of cancer stem cells. Their deregulation is a hallmark of different cancers types including breast cancer. Despite the growing evidence for their involvement in breast cancer, understanding the interplay between miRNAs and their targets leading to the disease remains largely unknown. Here, we provide a comprehensive story on miRNA signatures of breast cancer, miRNAs in breast cancer stem cells, metastamirs (i.e., metastasis regulatory miRNAs), circulating miRNAs as invasive blood-based biomarkers, and oncomiRs and oncosupressor miRNAs associated with breast cancer. Furthermore, we provide biological insights on their regulation by various mechanisms including genomic alterations and demonstration of a complicated feedback network between miRNAs and epigenetic regulators forming an epigenetics-miRNA regulatory circuit whose disruption may underlie the cause of breast cancer. Mol Cancer Res; 11(4); 315-28. Ó2013 AACR.

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The Oncogenic Role of miR-155 in Breast Cancer

Cited by 253 publications

References 88 publications

STAT5-mediated expression of oncogenic miR-155 in cutaneous T-cell lymphoma

STAT5-mediated expression of oncogenic miR-155 in cutaneous T-cell lymphoma

Oxidative Stress: Noxious but Also Vital

Genomic and Epigenomic Cross-talks in the Regulatory Landscape of miRNAs in Breast Cancer

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