The Roles of MicroRNAs in the Cancer Invasion-Metastasis Cascade

Le, Xiao Feng; Merchant, Omar; Bast, Robert C.; Calin, George A.

doi:10.1007/s12307-010-0037-4

Cited by 83 publications

(62 citation statements)

References 127 publications

(145 reference statements)

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“…MicroRNAs (miRNAs) play critical roles in this multi-step process, both promoting and suppressing metastasis (79). Specific miRNA can cause cancer cells to invade and metastasize (88).…”

Section: Metastasis To Other Benign Cns Tumorsmentioning

confidence: 99%

Tumor-to-tumor metastasis of the central nervous system

Erdoğan¹,

Aydin²,

Taşdemiroğlu³

2014

Turkish Neurosurgery

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Tumor-to-tumor metastasis is a well recognized phenomenon. Although any tumor may be potential recipient of metastasis, renal cell carcinoma and meningioma are the most common malignant and benign recipients, respectively, whereas the lung and breast are the most common metastatic donors respectively, in both settings. Patients with hereditary cancer syndromes may be at higher risk for the development of tumor-to-tumor metastases. The most common pattern of tumor-to-tumor metastasis for intracranial neoplasms is the type in which an aggressive high-grade malignancy serves as the source of tumor and a more indolent neoplasm serves as the recipient tumor. The development of tumor metastasis from a second primary malignancy is uncommon and remains biologically puzzling. Its low incidence has made its full biological characterization evasive. Although rare, neurosurgeons should be aware of the entity of tumor-to-tumor metastasis. KeywoRds: Tumor, Metastasis, Central nervous system ÖZTümörden tümöre metastaz, iyi bilinen bir fenomendir. Herhangi bir tümör, metastazlar için potansiyel hedef olsa da en sık yayıldıkları malign ve benign tümörler sırasıyla renal hücreli karsinom ve menenjiyomlardır, en sık kaynaklandıkları bölgeler ise akciğer ve memedir. Herediter kanser sendromlarına sahip olan hastalar tümörden tümöre metastaz gelişimi açısından daha fazla risk taşıyabilirler. İntrakranial neoplazilerde tümörden tümöre metastazların en sık görülen şekli, saldırgan ve yüksek evreli bir tümörün daha iyi huylu bir tümöre metastazı ile olandır. Tümör metastazının ikinci bir primer malign tümörden gelişmesi az görülür ve biyolojik olarak halen şaşırtıcıdır. Bu durumun insidansının düşük olması biyolojik tanımlamanın tam olarak yapılmasını da zorlaştırmaktadır. Nadir olsa bile nöroşirürjiyenler, bir antite olarak tümörden tümöre metastaz hakkında bilgi sahibi olmalıdırlar.

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“…MicroRNAs (miRNAs) play critical roles in this multi-step process, both promoting and suppressing metastasis (79). Specific miRNA can cause cancer cells to invade and metastasize (88).…”

Section: Metastasis To Other Benign Cns Tumorsmentioning

confidence: 99%

Tumor-to-tumor metastasis of the central nervous system

Erdoğan¹,

Aydin²,

Taşdemiroğlu³

2014

Turkish Neurosurgery

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Section: Introductionmentioning

confidence: 99%

“…The metastatic process of cancer cells is complicated and consists of multiple steps, including detachment, local invasion, motility, angiogenesis, extravasation, and growth in distant organs (2). Better elucidating the mechanisms of metastasis is important for improving the therapeutic efficiencies of gastric cancer (1,2). v-ets erythroblastosis virus E26 oncogene homolog 1 (Ets1) is a member of the Ets transcription factor family that participates in the migration, invasion, and angiogenesis of cancer cells (3).…”

Section: Introductionmentioning

confidence: 99%

miRNA-145 Targets v-ets Erythroblastosis Virus E26 Oncogene Homolog 1 to Suppress the Invasion, Metastasis, and Angiogenesis of Gastric Cancer Cells

Zheng

et al. 2013

Molecular Cancer Research

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Recent evidence shows that v-ets erythroblastosis virus E26 oncogene homolog 1 (Ets1) is implicated in tumor development and progression. However, the clinical potentials and underlying mechanisms of Ets1 in gastric cancer progression and metastasis remain largely unknown. In this study, Ets1 immunostaining was identified in 56 of 84 (66.7%) gastric cancer tissues, which was correlated with tumor invasion and metastasis. In gastric cancer specimens and cell lines, miRNA-145 (miR-145) was downregulated and inversely correlated with Ets1 expression. Bioinformatics analysis and luciferase reporter assay revealed that miR-145 directly targeted the 3 0 -untranslated region (3 0 -UTR) of Ets1 mRNA. Overexpression or knockdown of miR-145 responsively altered both the mRNA and protein levels of Ets1 and its downstream genes, matrix metalloproteinase (MMP-1)-1 and -9, in gastric cancer cell lines SGC-7901 and MKN-45. Ectopic expression of miR-145 suppressed the invasion, metastasis, and angiogenesis of SGC-7901 and MKN-45 cells in vitro and in vivo. In addition, the effects of miR-145 on Ets1 expression, migration, invasion, and angiogenesis were rescued by restoration of Ets1 expression in these cells. Furthermore, anti-miR-145 inhibitor promoted the migration, invasion, and angiogenesis, whereas siRNAmediated Ets1 knockdown phenocopied the effects of miR-145 overexpression in gastric cancer cells. These results show that miR-145 suppresses Ets1 expression via the binding site in the 3 0 -UTR, thus inhibiting the invasion, metastasis, and angiogenesis of gastric cancer cells. Mol Cancer Res; 11(2); 182-93. Ó2012 AACR.

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“…The upregulation of HIST1H4 can be associated with increased Notch1 stimulation, again connected to cancer metastasis, together with angiogenesis and NF-B production [30,44]; NF-B in turn contributes to the progression of colorectal cancer by regulating cell proliferation, angiogenesis and tumor metastasis [45]. Micro-RNA's block mRNA translation and thus impede the synthesis of specific proteins by recruiting the micro-RNA-induced silencing complex (miRISC) to target mRNAs [46]; downregulation of micro-RNA 222 and 644a thus increases KIT and -actin protein expression, respectively, thereby promoting endothelial cell proliferation and migration (angiogenesis) [36,47] and tumor cell invasiveness and motility [34]. -actin can be upregulated through the IL-6 receptor pathway as well: the increased IL-6 expression after quorum sensing peptide treatment, as observed with our cytokine array, activates -actin phosphorylation, again promoting tumor cell migration [48].…”

Section: Discussionmentioning

confidence: 99%

“…MicroRNA 222 is also highly expressed in endothelial cells, possessing anti-angiogenic properties through its targets c-kit (mast/stem cell growth factor receptor kit, CD117), p27Kip1, p57Kip2 (cyclin-dependent kinase inhibitor 1C) and cyclin G1 [36]. The downregulation after quorum sensing peptide addition thus initiates angiogenesis.…”

Section: Angiogenesis Confirms Metastatic Potential Of Quorum Sensingmentioning

confidence: 99%

Crosstalk between the microbiome and cancer cells by quorum sensing peptides

et al. 2015

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Highlights• Some quorum sensing peptides promote colon cancer cell invasion and angiogenesis.• Quorum sensing peptide Phr0662 influences tumor progression by EGFR targeting.• Cytokine profiles confirm the peptide's stimulatory effect on metastasis in vitro.• The microbiome-mammals crosstalk may explain the microbiome's effect on health. ABSTRACTTo date, the precise role of the human microbiome in health and disease states remains largely

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The Roles of MicroRNAs in the Cancer Invasion-Metastasis Cascade

Cited by 83 publications

References 127 publications

Tumor-to-tumor metastasis of the central nervous system

Tumor-to-tumor metastasis of the central nervous system

miRNA-145 Targets v-ets Erythroblastosis Virus E26 Oncogene Homolog 1 to Suppress the Invasion, Metastasis, and Angiogenesis of Gastric Cancer Cells

Crosstalk between the microbiome and cancer cells by quorum sensing peptides

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