MicroRNA-210 and its theranostic potential

Ren, Chun‐Xia; Leng, Rui‐Xue; Fan, Yin‐Guang; Pan, Hai‐Feng; Wu, Changhao; Ye, Dong‐Qing

doi:10.1080/14728222.2016.1206890

Cited by 18 publications

(18 citation statements)

References 138 publications

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“…Additionally, there is an intriguingly low cancer incidence in human patients with Huntington's disease and a body of work examining the role of mutant and wild-type huntingtin protein in cancer development and progression (46). Marked upregulation of this "master" hypoxamiR in these three canine high-grade glioma cell lines serves as confirmation of experimental hypoxia induction and also confirms that glioma-bearing canine patients may be useful models for studying therapies directed at this target (72,73).…”

Section: Mir-210: Upregulated In Hypoxia In Canine High-grade Glioma mentioning

confidence: 63%

Differential Expression of miRNAs in Hypoxia (“HypoxamiRs”) in Three Canine High-Grade Glioma Cell Lines

et al. 2020

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Dogs with spontaneous high-grade gliomas increasingly are being proposed as useful large animal pre-clinical models for the human disease. Hypoxia is a critical microenvironmental condition that is common in both canine and human high-grade gliomas and drives increased angiogenesis, chemo-and radioresistance, and acquisition of a stem-like phenotype. Some of this effect is mediated by the hypoxia-induced expression of microRNAs, small (∼22 nucleotides long), non-coding RNAs that can modulate gene expression through interference with mRNA translation. Using an in vitro model with three canine high-grade glioma cell lines (J3T, SDT3G, and G06A) exposed to 72 h of 1.5% oxygen vs. standard 20% oxygen, we examined the global "hypoxamiR" profile using small RNA-Seq and performed pathway analysis for targeted genes using both Panther and NetworkAnalyst. Important pathways include many that are well-established as being important in glioma biology, general cancer biology, hypoxia, angiogenesis, immunology, and stem-ness, among others. This work provides the first examination of the effect of hypoxia on miRNA expression in the context of canine glioma, and highlights important similarities with the human disease.

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Section: Mir-210: Upregulated In Hypoxia In Canine High-grade Glioma mentioning

confidence: 63%

Differential Expression of miRNAs in Hypoxia (“HypoxamiRs”) in Three Canine High-Grade Glioma Cell Lines

et al. 2020

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“…miR-210, which is a regulator of several cellular functions, dependent on or independent of hypoxia signaling, is involved in numerous biological processes of numerous tumors throughout the human body (42). miR-210 has been identified as an activator of tumor initiation and development, and its high levels are associated with a negative clinical outcome (43). It has been reported to be involved in cell survival, differentiation, angiogenesis, metabolism and cell cycle control (15,44).…”

Section: Discussionmentioning

confidence: 99%

Exosomal microRNA‑210 is a potentially non‑invasive biomarker for the diagnosis and prognosis of glioma

2020

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MicroRNAs (miRs) transferred by exosomes can function as non-invasive potential biomarkers for the diagnosis and prognosis in various types of cancer. The present study examined the diagnostic and prognostic value of serum exosomal-(exo-)miR-210 levels in association with hypoxic conditions in patients with glioma. Serum levels of exo-miR-210 were determined by quantitative PCR in samples obtained from patients with glioma. Patients were divided into low-and high-expression exo-miR-210 groups according to the median expression value. Statistical analyses were conducted to examine the potential value of exo-miR-210 in predicting the diagnosis and prognosis of patients with glioma. A significant increase in serum exo-miR-210 levels was observed in patients with glioma compared with healthy controls. Additionally, the expression levels of exo-miR-210 were increased with ascending pathological grades. Furthermore, expression levels of miR-210 in serum exosomes from patients with glioblastoma were markedly decreased following surgery and upregulated once more at the recurrences of primary tumors, indicating that exo-miR-210 could reflect alterations in malignant glioma loads. In addition, Kaplan-Meier analysis was performed to analyze overall survival (OS) time. Patients with malignant glioma with high exo-miR-210 expression exhibited a poorer OS compared with patients with low expression. Importantly, univariate and multivariate Cox regression analysis revealed that the expression levels of exo-miR-210 in glioma serum samples were independently associated with OS. Finally, increased serum exo-miR-210 expression was positively associated with high levels of hypoxia-inducible factor 1a and reflected hypoxia in patients with glioma. In conclusion, serum levels of exo-miR-210 may serve as a diagnostic, prognostic and hypoxic biomarker to reflect glioma status and hypoxic signatures.

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“…The precursor of miR-210 forms a stem-loop structure and is located within the intron region of AK123483 gene, which is located on chromosome 11p15.5 (19). The gene sequence of miR-210 is evolutionarily conserved between different species, indicating its functional importance (20,21). Convincing evidence suggests that miR-210 is widely expressed in multiple tissues and cells, including hematopoietic stem cells, numerous cancer cells, myeloid cells and lymphocytes (22)(23)(24)(25).…”

Section: Discussionmentioning

confidence: 99%

HBV infection suppresses the expression of inflammatory macrophage miR‑210

Bian

Wang

et al. 2018

Mol Med Report

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It has been previously reported that hepatitis B e-antigen (HBeAg) induces microRNA (miR)-155 expression and promotes liver injury by increasing inflammatory cytokine production in macrophages. Moreover, it was previously demonstrated that miR-210 alleviates lipopolysaccharide-stimulated proinflammatory cytokine production in macrophages. In addition, accumulating evidence suggests that miR-210 is able to suppress hepatitis B virus (HBV) replication in HepG2.2.15 cells. However, it remains unclear whether miR-210, similar to miR-155, affects the progress of hepatitis B by regulating macrophage function. Reverse transcription-quantitative polymerase chain reaction analysis was used to detect miR-210 levels in serum and cells. HBV-associated antigens stimulated different types of macrophages and facilitated the observation of the effects of these antigens on miR-210 expression in macrophages. Co-culture of peripheral blood monocytes from healthy controls and the serum of patients with chronic hepatitis B (CHB) was conducted to evaluate the effect of HBV-associated elements in the serum on the expression of the macrophage miR-210 in vivo. It was observed that miR-210 expression levels were decreased in the peripheral blood monocytes (PBMs) and serum of patients with CHB and negatively associated with serum alanine aminotransferase and aspartate aminotransferase, but not other clinical parameters including hepatitis B surface antigen (HBsAg), HBeAg, anti-HBe antibody (HBeAb) and hepatitis B core antibody (HBcAb) and HBV-DNA. Notably, it was demonstrated that miR-210 expression was not affected by treatment with HBV-associated antigens in different types of macrophages. Notably, the serum of patients with CHB was able to markedly downregulate the miR-210 expression of PBMs in healthy controls. These findings suggested that, unlike the induction of miR-155 by HBeAg, there may be certain other elements, apart from HBV-associated antigens, regulating miR-210 levels in the serum and PBMs of patients with CHB that affect macrophage activation.

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MicroRNA-210 and its theranostic potential

Cited by 18 publications

References 138 publications

Differential Expression of miRNAs in Hypoxia (“HypoxamiRs”) in Three Canine High-Grade Glioma Cell Lines

Differential Expression of miRNAs in Hypoxia (“HypoxamiRs”) in Three Canine High-Grade Glioma Cell Lines

Exosomal microRNA‑210 is a potentially non‑invasive biomarker for the diagnosis and prognosis of glioma

HBV infection suppresses the expression of inflammatory macrophage miR‑210

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