MiR-30a: A Novel Biomarker and Potential Therapeutic Target for Cancer

Jiang, Linhong; Zhang, Heda; Tang, Jinhai

doi:10.1155/2018/5167829

Cited by 73 publications

(60 citation statements)

References 75 publications

(101 reference statements)

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“…[5,20,21] MicroRNAs (miRNAs) are short non-coding RNA approximately 19-25 nucleotides in length, which directly bind to the 3 0 -UTR of target mRNAs to regulate gene expression, either through degradation of the RNA or translation inhibition. [22,23] MiRNAs participate in diverse molecular and cellular processes, such as cellular migration/invasion, cell growth, apoptosis and signal transduction. MiRNAs dysregulation is a hallmark of many cancers, including glioblastoma, and they can be classified into tumour-suppressive miRNAs and onco-miRNAs.…”

Section: Introductionmentioning

confidence: 99%

MiRNA-7 enhances erlotinib sensitivity of glioblastoma cells by blocking the IRS-1 and IRS-2 expression

Alamdari-Palangi

Amini

Karami

2020

Journal of Pharmacy and Pharmacology

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Objectives Down‐regulation of miRNA‐7 is correlated with over‐expression of IRS‐1 and IRS‐2 proteins, the upstream regulators of IGF‐1R/Akt pathway, in glioblastoma cells. In this study, the effect of miRNA‐7 on expression of IRS‐1 and IRS‐2 and sensitivity of the U373‐MG glioblastoma cells to erlotinib was explored. Methods After miRNA‐7 transfection, the expression of IRS‐1 and IRS‐2 mRNAs was measured by RT‐qPCR. Trypan blue assay was used to assess the effect of miRNA‐7 on cell proliferation. The effects of miRNA‐7 and erlotinib, alone and in combination, on cell survival and apoptosis were measured using MTT assay and ELISA cell death assay, respectively. Key findings Our data showed that miRNA‐7 markedly inhibited the expression of IRS‐1 and IRS‐2 in a time‐dependent manner, inhibited the proliferation of glioblastoma cells and enhanced apoptosis (P < 0.05, relative to control). Pretreatment with miRNA‐7 synergistically inhibited the cell survival rate and decreased the IC50 of erlotinib. Furthermore, miRNA‐7 significantly augmented the apoptotic effect of erlotinib. Conclusions Our data propose that inhibition of IRS‐1 and IRS‐2 by miRNA‐7 can effectively induce apoptosis and sensitize glioblastoma cell to EGFR‐TKIs. Therefore, miRNA‐7 may be a potential therapeutic target in patients with glioblastoma.

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Section: Introductionmentioning

confidence: 99%

MiRNA-7 enhances erlotinib sensitivity of glioblastoma cells by blocking the IRS-1 and IRS-2 expression

Alamdari-Palangi

Amini

Karami

2020

Journal of Pharmacy and Pharmacology

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“…Numerous pieces of evidence show that abnormal expression of miRNAs and their regulation play important roles in the initiation and progression of human cancers, such as esophageal carcinoma, hepatocellular carcinoma and breast carcinoma . Some miRNAs, such as miR‐30a, are able to affect many types of malignancies and can be used as biomarkers for these tumors . To date, multiple miRNAs have been shown to have vital functions in the development of NSCLC, but few of these miRNAs could be a candidate for targeted therapy, and the specific underlying mechanisms for their effects in the tumorigenesis and progression of NSCLC are still not understood.…”

Section: Introductionmentioning

confidence: 99%

“…9 Some miRNAs, such as miR-30a, are able to affect many types of malignancies and can be used as biomarkers for these tumors. 10 To date, multiple miRNAs have been shown to have vital functions in the development of NSCLC, 11,12 but few of these miRNAs could be a candidate for targeted therapy, 13 and the specific underlying mechanisms for their effects in the tumorigenesis and progression of NSCLC are still not understood.…”

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confidence: 99%

MicroRNA‐331‐3p inhibits epithelial‐mesenchymal transition by targeting ErbB2 and VAV2 through the Rac1/PAK1/β‐catenin axis in non‐small‐cell lung cancer

Zhu

Liu

et al. 2019

Cancer Science

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MicroRNAs have been reported to play critical roles in the regulation of non‐small‐cell cancer (NSCLC) development, but the role of microRNA (miR)‐331‐3p in NSCLC is still unclear. In this study, the expression levels of miR‐331‐3p in NSCLC tumor tissues and adjacent normal tissues were examined by quantitative RT‐PCR, and the relationship between miR‐331‐3p expression and patient clinicopathological characteristics was analyzed. The effects of miR‐331‐3p on epithelial‐mesenchymal transition (EMT), migration, and metastasis of NSCLC cells were determined in vitro and vivo. Direct functional targets of miR‐331‐3p were identified by luciferase reporter assay, western blot assay, immunohistochemical staining, and rescue assay. The downstream pathway regulated by miR‐331‐3p was identified by immunofluorescence, immunoprecipitation, and Rac1 activity examination. Our results showed that miR‐331‐3p was significantly downregulated in NSCLC tumor tissues and was correlated with clinicopathological characteristics, and miR‐331‐3p could be an independent prognostic marker for NSCLC patients. Furthermore, miR‐331‐3p significantly suppressed EMT, migration and metastasis of NSCLC cells in vitro and in vivo. Both ErbB2 and VAV2 were direct functional targets of miR‐331‐3p. The activities of Rac1, PAK1, and β‐catenin were regulated by miR‐331‐3p through ErbB2 and VAV2 targeting. These results indicated that miR‐331‐3p suppresses EMT, migratory capacity, and metastatic ability by targeting ErbB2 and VAV2 through the Rac1/PAK1/β‐catenin axis in NSCLC.

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“…The miR‐30a has been demonstrated to play an important role in biological processes, including cancer proliferation, metastasis, and apoptosis. Moreover, miR‐30 is also involved in several signal pathways to regulate autophagy or drug susceptibility (Jiang, Zhang, & Tang, ). The previous study reported that miR‐30 regulated Toll‐like receptor (TLR)/MyD88 activation and cytokine expression in THP‐1 cells during Mycobacterium tuberculosis infection (Wu, Sun, & Dai, ).…”

Section: Discussionmentioning

confidence: 99%

Exosomes from EV71‐infected oral epithelial cells can transfer miR‐30a to promote EV71 infection

Wang¹,

Zhang

Song³

et al. 2020

Oral Diseases

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Objective As an extracellular vesicle, exosomes can release from virus‐infected cells containing various viral or host cellular elements and could stimulate recipient's cellular response. Enterovirus 71 (EV71), a single‐strand positive‐sense RNA virus, is known to cause hand, foot, and mouth disease (HFMD) in children and bring about severe clinical diseases. Methods Separated the human oral epithelial cells (OE cells) from normal buccal mucosa through enzyme digestion. Performed a comprehensive miRNA profiling in exosomes from EV71‐infected OE cells through deep small RNA‐seq. Using the Human Antiviral Response RT Profiler PCR Array profiles to explore the interactions of innate immune signaling networks with exosomal miR‐30a. Knocked out the MyD88 gene in macrophages using CRISPR/Cas9‐mediated genome editing method. Results Our study demonstrated that the miR‐30a was preferentially enriched in exosomes that released from EV71‐infected human oral epithelial cells through small RNA‐seq. We found that the transfer of exosomal miR‐30a to macrophages could suppress type Ⅰ interferon response through targeting myeloid differentiation factor 88 (MyD88) and subsequently facilitate the viral replication. Conclusions Exosomes released from EV71‐infected OE cells selectively packaged high level of miR‐30a that can be functionally transferred to the recipient macrophages resulted in targeting MyD88 and subsequently inhibited type I interferon production in receipt cells, thus promoting the EV71 replication.

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MiR-30a: A Novel Biomarker and Potential Therapeutic Target for Cancer

Cited by 73 publications

References 75 publications

MiRNA-7 enhances erlotinib sensitivity of glioblastoma cells by blocking the IRS-1 and IRS-2 expression

MiRNA-7 enhances erlotinib sensitivity of glioblastoma cells by blocking the IRS-1 and IRS-2 expression

MicroRNA‐331‐3p inhibits epithelial‐mesenchymal transition by targeting ErbB2 and VAV2 through the Rac1/PAK1/β‐catenin axis in non‐small‐cell lung cancer

Exosomes from EV71‐infected oral epithelial cells can transfer miR‐30a to promote EV71 infection

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