miRNA-based biomarkers, therapies, and resistance in Cancer

He, Boxue; Zhao, Zhenyu; Cai, Qidong; Zhang, Yuqian; Zhang, Pengfei; Shi, Shuai; Xie, Hui; Xiong, Ping; Yin, Wei; Tao, Yongguang; Wang, Xiang

doi:10.7150/ijbs.47203

Cited by 310 publications

(204 citation statements)

References 229 publications

(222 reference statements)

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“…In various contexts, a specific miRNA could simultaneously produce competing oncogenic and tumor suppressive effects by the modulation of oncogenic or tumor suppressive mRNAs, respectively [ 43 ]. Additionally, miRNAs can modulate tumor-modifying extrinsic factors such as cancer-immune system interactions, stromal cell interactions, and sensitivity to therapy [ 44 , 45 , 46 ]. It likely the balance between these processes which determines the net outcome of whether a specific miRNA produces an oncogenic or tumor suppressive effect.…”

Section: Discussionmentioning

confidence: 99%

MiR-181 Family Modulates Osteopontin in Glioblastoma Multiforme

Marisetty

Wei

Kong

et al. 2020

Cancers

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MiRNAs can silence a wide range of genes, which may be an advantage for targeting heterogenous tumors like glioblastoma. Osteopontin (OPN) plays both an oncogenic role in a variety of cancers and can immune modulate macrophages. We conducted a genome wide profiling and bioinformatic analysis to identify miR-181a/b/c/d as potential miRNAs that target OPN. Luciferase assays confirmed the binding potential of miRNAs to OPN. Expression levels of miR-181a/b/c/d and OPN were evaluated by using quantitative real-time PCR and enzyme-linked immunosorbent assay in mouse and human glioblastomas and macrophages that showed these miRNAs were downregulated in Glioblastoma associated CD11b+ cells compared to their matched blood CD14b+ cells. miRNA mimicking and overexpression using lentiviruses showed that MiR-181a overexpression in glioblastoma cells led to decreased OPN production and proliferation and increased apoptosis in vitro. MiR-181a treatment of immune competent mice bearing intracranial glioblastoma demonstrated a 22% increase in median survival duration relative to that of control mice.

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Section: Discussionmentioning

confidence: 99%

MiR-181 Family Modulates Osteopontin in Glioblastoma Multiforme

Marisetty

Wei

Kong

et al. 2020

Cancers

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“…Calin et al reported that more than 50% of miRNA genes are located in genomic regions associated with cancer 9 . It is now well established from a variety of studies that miRNAs are involved in tumor progression as oncogenes or tumor suppressors 10 , 11 . In addition, miRNAs also play essential regulatory roles in inflammatory and immune responses 12 .…”

Section: Introductionmentioning

confidence: 99%

Enforced expression of miR-92b blunts E. coli lipopolysaccharide-mediated inflammatory injury by activating the PI3K/AKT/β-catenin pathway via targeting PTEN

Jiang¹,

Yang²,

Song³

et al. 2021

Int. J. Biol. Sci.

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Endometritis is a reproductive disorder characterized by an inflammatory response in the endometrium, which causes significant economic losses to the dairy farming industry. MicroRNAs (miRNAs) are implicated in the inflammatory response and immune regulation following infection by pathogenic bacteria. Recent miRNA microarray analysis showed an altered expression of miR-92b in cows with endometritis. In the present study, we set out to investigate the regulatory mechanism of miR-92b in endometritis. Here, qPCR results first validated that miR-92b was down-regulated during endometritis. And then, bovine endometrial epithelial cells (BEND cells) stimulated by high concentration of lipopolysaccharide (LPS) were employed as an in vitro inflammatory injury model. Our data showed that overexpression of miR-92b significantly suppressed the activation of Toll-like receptor 4 (TLR4) and nuclear factor-κB (NF‐κB) in LPS-stimulated BEND cells, thereby reducing pro-inflammatory cytokines release and inhibiting cell apoptosis. Looking into the molecular mechanisms of regulation of inflammatory injury by miR-92b, we observed that overexpression of miR-92b restrained TLR4/NF‐κB by activating the phosphatidylinositol 3-kinase/protein kinase B (PI3K/AKT)/β-catenin pathway. Furthermore, the luciferase reporter assay suggested that miR-92b targeted inhibition of phosphatase and tensin homolog (PTEN), an inhibitor of the PI3K/AKT/β-catenin pathway. Importantly, in vivo experiments confirmed that up-regulation of miR-92b attenuated the pathological injury in an experimental murine model of LPS-induced endometritis. Collectively, these findings show that enforced expression of miR-92b alleviates LPS-induced inflammatory injury by activating the PI3K/AKT/β-catenin pathway via targeting PTEN, suggesting a potential application for miR-92b-based therapy to treat endometritis or other inflammatory diseases.

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“…The miRNA microarray is one of the most common methods of screening disease-associated miRNAs, and several studies using this technology have revealed aberrant miRNA expression in human malignant tumors ( 10 , 29 ), including CRC ( 17 ). Volinia et al ( 29 ) used miRNA microarrays to study the expression patterns of miRNAs in 540 tumor tissues and found that miRNAs are differentially expressed in non-cancer and cancer tissues.…”

Section: Discussionmentioning

confidence: 99%

MicroRNA‑142‑3p suppresses cell proliferation, invasion and epithelial‑to‑mesenchymal transition via RAC1‑ERK1/2 signaling in colorectal cancer

et al. 2021

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Aberrant expression of microRNAs (miRNAs/miRs) is associated with the initiation and progression of colorectal cancer (CRC), but how they regulate colorectal tumorigenesis is still unknown. The present study was designed to investigate the expression profile of miRNAs in human CRC tissues, and to reveal the molecular mechanism of miRNA-142-3p in suppressing colon cancer cell proliferation. The expression of miRNA was examined using an Exiqon miRNA array. Bioinformatics was used to predict the target genes of differentially expressed miRNAs and to analyze their biological function in CRC. The effect of miR-142-3p in colon cancer cells was evaluated in vitro using cell proliferation, colony formation and Transwell assays. Dual-luciferase reporter gene assays were performed to investigate the association between miR-142-3p and Rac family small GTPase 1 (RAC1). The effect of miR-142-3p regulation on colon cancer proliferation was assessed through western blotting and quantitative polymerase chain reaction analysis. Compared with their expression in adjacent non-cancer mucosal tissues, 76 miRNAs were upregulated and 102 miRNAs were downregulated in CRC. One of the most significantly and differentially regulated miRNAs was miR-142-3p, which was downregulated in 81.0% (51/63) of primary CRC tissues. After transfection of miR-142-3p mimics into colon cancer cells, proliferation and colony formation were decreased, and migration and invasion were markedly suppressed. RAC1 was a possible target of miR-142-3p, which was confirmed by dual-luciferase reporter assay. Transfection of miR-142-3p mimics decreased the levels of RAC1 and suppressed epithelial-to-mesenchymal transition in colon cancer cells. The phosphorylation of extraceullar signal-regulated kinase (ERK) was decreased significantly by the inhibition of RAC1 or transfection of miR-142-3p mimics in colon cancer cells. In conclusion, aberrant miRNAs are implicated in CRC. Decreased expression of miR-142-3p may be associated with CRC tumorigenesis via Rac1-ERK signaling.

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miRNA-based biomarkers, therapies, and resistance in Cancer

Cited by 310 publications

References 229 publications

MiR-181 Family Modulates Osteopontin in Glioblastoma Multiforme

MiR-181 Family Modulates Osteopontin in Glioblastoma Multiforme

Enforced expression of miR-92b blunts E. coli lipopolysaccharide-mediated inflammatory injury by activating the PI3K/AKT/β-catenin pathway via targeting PTEN

MicroRNA‑142‑3p suppresses cell proliferation, invasion and epithelial‑to‑mesenchymal transition via RAC1‑ERK1/2 signaling in colorectal cancer

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