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Background and study aims

Although the function of microRNA21 (miR-21) in the invasion and metastasis of colon cancer has been extensively studied, the mechanisms of invasion and migration related pathways between and its targets are still not elucidated. This study explored the mechanisms of the pathway between miR-21 and the target genes in vitro and in vivo.

Materials and methods

We transfected pmiRZip21 or Leti3 into colon cancer cells. The levels of miR-21 expression, mRNA transcription and protein of target genes were analysed by TaqMan microRNA assays, RT-PCR and western blot, respectively. Scratch migration and trans-well assays were used to evaluate metastasis and invasion. To build a subcutaneous tumour animal model, detect the level of miR-21 and the target genes and then identify the mechanisms in vivo.

Results

MiR-21 expression levels in colon cancer cells transfected with pmiRZip21 in vivo or in vitro were decreased (P < 0.05). The mRNA and protein levels of TIMP-3 and RECK were up-regulated after inhibiting miR-21 in vitro and in vivo (P < 0.05), but those of BMPR-II and PCDH17 were not. In pmiRZip21-transfected colon cancer cells, invasion and migration were significantly decreased both in vitro and vivo (P < 0.05).

Conclusions

Up-regulation of TIMP-3 and RECK, by inhibiting miR-21 expression can decrease tumour invasion and metastasis ability in vitro and in vivo, and has potential as a possible target site in anti-tumour therapy. More effects in vivo have to be investigated in further research."xsd:string
http://purl.uniprot.org/citations/31558368http://purl.org/dc/terms/identifier"doi:10.1016/j.ajg.2019.07.003"xsd:string
http://purl.uniprot.org/citations/31558368http://purl.uniprot.org/core/author"Jiang T."xsd:string
http://purl.uniprot.org/citations/31558368http://purl.uniprot.org/core/author"Gao C."xsd:string
http://purl.uniprot.org/citations/31558368http://purl.uniprot.org/core/author"Liu T."xsd:string
http://purl.uniprot.org/citations/31558368http://purl.uniprot.org/core/author"Lin Y."xsd:string
http://purl.uniprot.org/citations/31558368http://purl.uniprot.org/core/author"Wei Y."xsd:string
http://purl.uniprot.org/citations/31558368http://purl.uniprot.org/core/author"Wang D."xsd:string
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http://purl.uniprot.org/citations/31558368http://purl.uniprot.org/core/author"Wang X."xsd:string
http://purl.uniprot.org/citations/31558368http://purl.uniprot.org/core/author"Zhu L."xsd:string
http://purl.uniprot.org/citations/31558368http://purl.uniprot.org/core/author"Wang P."xsd:string
http://purl.uniprot.org/citations/31558368http://purl.uniprot.org/core/author"Qi F."xsd:string
http://purl.uniprot.org/citations/31558368http://purl.uniprot.org/core/date"2019"xsd:gYear
http://purl.uniprot.org/citations/31558368http://purl.uniprot.org/core/name"Arab J Gastroenterol"xsd:string
http://purl.uniprot.org/citations/31558368http://purl.uniprot.org/core/pages"127-134"xsd:string
http://purl.uniprot.org/citations/31558368http://purl.uniprot.org/core/title"Up-regulation of TIMP-3 and RECK decrease the invasion and metastasis ability of colon cancer."xsd:string
http://purl.uniprot.org/citations/31558368http://purl.uniprot.org/core/volume"20"xsd:string
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