microRNA Therapeutics in Cancer — An Emerging Concept

Shah, Maitri; Ferrajoli, Alessandra; Sood, Anil K.; López-Berestein, Gabriel; Calin, George A.

doi:10.1016/j.ebiom.2016.09.017

Cited by 385 publications

(346 citation statements)

References 94 publications

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“…Although the roles of HGF and VEGF have been discovered, the mechanisms underlying the up-regulation of HGF expression, especially in the tumorigenesis of GC, remain largely unknown. microRNAs (miRNAs) are a class of small noncoding RNAs (~22 bp) that are believed to regulate gene expression by directly binding with the 3'UTR of target mRNAs, causing translational inhibition or mRNA degradation [16]. Some miRNAs are closely related to the tumor formation [17][18][19].…”

Section: Introductionmentioning

confidence: 99%

miR-26a/b Inhibit Tumor Growth and Angiogenesis by Targeting the HGF-VEGF Axis in Gastric Carcinoma

Si¹,

Zhang²,

Ning³

et al. 2017

Cell Physiol Biochem

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Background/Aims: Abnormal expression of HGF is found in various cancers and correlates with tumor proliferation, metastasis and angiogenesis. However, the regulatory mechanism of the HGF-VEGF axis remains unclear. Methods: The expression characteristic of HGF in human gastric cancer tissues was shown by an immunohistochemistry assay, and the expression levels of target protein were detected by Western blot. The relative levels of miR-26a/b and target mRNA were examined by qRT-PCR. We used bioinformatics tools to search for miRNAs that can potentially target HGF. A luciferase assay was used to confirm direct targeting. Furthermore, the functions of miR-26a/b and HGF were evaluated by cell proliferation and migration assays in vitro and by the mouse xenograft tumor model in vivo. Results: We found that the HGF protein was clearly increased while miR-26a/b were dramatically down-regulated in gastric cancer. miR-26a/b directly bind to the 3'-UTR of HGF mRNA at specific targeting sites. We demonstrated that the repression of the HGF-VEGF pathway by miR-26a/b overexpression suppressed gastric cancer cell proliferation and migration. Furthermore, miR-26a/b also showed an anti-tumor effect in the xenograft mouse model by suppressing tumor growth and angiogenesis. Conclusions: miR-26a/b could suppress tumor tumorigenesis and angiogenesis by targeting the HGF-VEGF axis and could serve as a potential treatment modality for targeted therapy in the clinical treatment of gastric cancer.

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Section: Introductionmentioning

confidence: 99%

miR-26a/b Inhibit Tumor Growth and Angiogenesis by Targeting the HGF-VEGF Axis in Gastric Carcinoma

Si¹,

Zhang²,

Ning³

et al. 2017

Cell Physiol Biochem

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“…Thus far, phase I and II clinical trials involving microRNA-based therapies, i.e. treatment of cancer patients with a liposome-formulated mimic of the tumor suppressor miR-34 (MRX34), have not yet yielded valuable drugs (18). However, it is conceivable that therapeutic approaches aimed at increasing plasma miR-499-5p levels will be developed in the future that can be of benefit for high risk cardiovascular disease patients.…”

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confidence: 99%

MicroRNA-499-5p: a therapeutic target in the context of cardiovascular disease

Hoekstra¹

2016

Ann. Transl. Med.

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“…Several miRs have been reported to have an important role in tumor metastasis (45)(46)(47). Furthermore, since miRs regulate multiple target genes simultaneously, miR-based therapy is expected to be more efficient than the traditional single target therapy (48,49). In the present study, miR-429 was shown to be an important regulator in tumor cell migration and invasion, which emphasized an essential role of miR-429 in regulating GC metastasis.…”

Section: Discussionmentioning

confidence: 64%

MicroRNA-429 inhibits gastric cancer migration and invasion through the downregulation of specificity protein 1

Yang

Liu

et al. 2017

Oncology Letters

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Abstract. microRNAs (miRs) have been reported to have an important role in tumorigenesis and tumor progression. Although miR-429 has been shown to be downregulated in gastric cancer (GC), the function of miR-429 in the metastasis of GC has yet to be investigated. In the present study, GC cells were transfected with miR-429, and reverse transcription-quantitative polymerase chain reaction, cell migration assays, cell invasion assays, western blot analysis and luciferase assays were conducted to investigate the role of miR-429 in GC cells. It was demonstrated that miR-429 expression was markedly increased following transfection of the cells with miR-429. Furthermore, miR-429 was shown to inhibit the migration and invasion of GC cell lines. In addition, this study provided evidence that miR-429 directly targets specificity protein 1 in GC cells. The results of the present study may enhance current knowledge regarding the molecular basis of cancer metastasis and provide a potential therapeutic strategy for GC.

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microRNA Therapeutics in Cancer — An Emerging Concept

Cited by 385 publications

References 94 publications

miR-26a/b Inhibit Tumor Growth and Angiogenesis by Targeting the HGF-VEGF Axis in Gastric Carcinoma

miR-26a/b Inhibit Tumor Growth and Angiogenesis by Targeting the HGF-VEGF Axis in Gastric Carcinoma

MicroRNA-499-5p: a therapeutic target in the context of cardiovascular disease

MicroRNA-429 inhibits gastric cancer migration and invasion through the downregulation of specificity protein 1

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