When stratified by cancer type, there were no significant cancer risk changes for lung cancer, breast cancer or colorectal cancer when miR-149 T allele was included.
Among those that engaged in smoke inhalation, miR-149 CT/CC and miR-605 AG/GG genotype carriers had increased susceptibilities to colorectal cancer (OR = 1.90, 95% CI: 1.11-3.25) and gastric cancer (OR = 1.87, 95% CI: 1.03-3.42), respectively.
We investigated the distribution of sequence variants of miR-146a, miR-196a2, miR-499 and miR-149 in colorectal cancer (CRC) and their effect on miRNA expression.Each variant was identified with HRM.
Our data suggest that, as a methylation-sensitive miRNA, miR-149 may play an important role as a tumour suppressor in CRC, which has prognostic and therapeutic implications.
This study aims to quantify the strength of the correlation between the four common polymorphisms among microRNAs (hsa-mir-146a rs2910164, hsa-mir-149rs2292832, hsa-mir-196a2 rs11614913, and hsa-mir-499 rs3746444) and CRC risk.
In conclusion, the SNPs rs2292832 in miR-149 and rs895819 in pre-miR-27a were associated with CRC susceptibility, whereas rs11614913, rs2910164, and rs3746444 in miR-196a-2, miR-146a, and miR-499, respectively, were not.
In conclusion, the increased plasma GPC1<sup>+</sup> exosomes and reduced plasma miR-96-5p and miR-149 expression are specific markers for the diagnosis of CRC and targets for the therapy of CRC.
In conclusion, we identified a variety of miRNAs (miRNA-let-7, miR-34b/c, miR-146a, miR-603 and miR-149) gene polymorphisms that are associated with susceptibility to CRC.
This study further investigated the clinical significance of plasma GPC1<sup>+</sup> exosomes and plasma miR-96-5p and miR-149 levels in stage III CRC patients.
In this study, we investigated the association of hsa-mir-149rs2292832 C/T, hsa-mir-146a rs2910164 G/C and hsa-mir-196a2 rs11614913 C/T and explored their roles in clinicopathological features of CRC progression in an Eastern Tunisian cohort.
This study demonstrated that GACAT3 promotes tumor progression through competitive binding to miR-149 and suggests a promising new strategy for anti-CRC therapy.
Taken together, we determined that the p53/miR-149-3p/PDK2 signaling pathway can potentially be targeted with DCA treatment to overcome chemoresistant CRC.