Metastasis-related miRNAs are overexpressed in CTCs and corresponding plasma; miR-21 expression levels highly correlate in CTCs and plasma; and miR-21, miR-146a, and miR-210 are valuable plasma biomarkers for discriminating patients from healthy individuals.
MicroRNA-210 was also a significant predictor for overall survival (OS), metastasis free survival or distant relapse free survival (MFS/DRFS), and disease specific survival (DSS).
miR-210 was significantly higher in N1 PCa compared with nonmetastatic PCa, whereas the metastatic tumor revealed a lower expression level of miR-210 than the primary tumor.
Accumulating evidence has revealed that various microRNAs are deregulated and involved in lung cancer development and metastasis. miR-210 is implicated in several cancer progression.
Accumulating evidence indicates that miRNAs contribute to tumorigenesis and cancer metastasis. microRNA-210 has been largely studied in the past several years and has been identified as a major miRNA induced under hypoxia.
Additionally, re-analysis of previously published expression data of two matching cohorts (<i>n</i> = 100, <i>n</i> = 255) supports an association of hsa-miR-128-3p with shortened disease-free survival (HR:2.48, <i>p</i> = 0.0033) and an upregulation of miR-7-5p (<i>p</i> = 0.0038; <i>p</i> = 0.039) and miR-210-3p (<i>p</i> = 0.031) in primary tumors of patients who experienced metastases.
Furthermore, the plasma level of miR-200a was significantly associated with the stage in surgery ( P = .035), and the high level of miR-210 expression was associated with internal organ metastasis (liver, lung, and brain; P = .024).
HIF-1α drives miR-210's overexpression and the resultant alteration of cellular processes, including cell cycle regulation, mitochondria function, apoptosis, angiogenesis and metastasis.
In addition, miR-210 upregulation more frequently occurred in osteosarcoma tissues with large tumor size (P = 0.02), poor response to preoperative chemotherapy (P = 0.008), and positive metastasis (P = 0.01).
In addition, genes encoding miRNA important for epithelial mesenchymal transition and other metastasis-related effects, such as mir-9, miR-34 and miR-210 can be good candidates for associating their DNA methylation profiles with CRC metastasis.
In addition, there was no significant association between serum miR-210 levels and age, sex, tumor size or existence of metastasis at diagnosis among the 34 CCC patients.
In multivariate analysis, miR-210 lost its statistically significant association with shorter disease-free survival and overall survival after adjusting for tumor size and tumor, node, metastasis stage.
In vivo xenograft assay and metastasis assay were performed to study the effects of miR-210 targeting E-cadherin on BCSCs growth and lung metastasis, and the tumors were assessed by immunohistochemistry and immunofluorescence.
Likewise, microRNA-210 transfection nearly totally inhibited tumor xenograft growth, proliferation and metastasis without obvious side effects in vivo.
Moreover, MYCBP expression was positively correlated with tumor volume, and metastasis was associated with the expression of miR-210-5p and TGF-α in our patient cohort.
Neutral sphingomyelinase 2 regulates exosomal microRNA secretion and promotes angiogenesis within the tumor microenvironment as well as metastasis; in particular, the exosomal miR-210 secretion by neutral sphingomyelinase 2 confers the formation of the tumor vessel network.
Only miR-138-5p upregulation was associated with higher survival rates. miR-335-5p, miR-301a-3p, and miR-210-3p were more highly expressed in patients with tumor metastasis and relapse. miR-138-5p, miR-146b-5p, and miR-218-5p expression were associated with higher disease-free survival (DFS) in treated patients.
Over-expressed microRNA-210 demonstrated a significantly higher risk of recurrence, metastasis and overall decreased survival rates for breast cancer patients.