It seemed that there was a high potential for highly expressed SNHG1 and lowly expressed miR-497/miR-195 to symbolize CRC patients' unfavorable prognosis (p < .05).
In addition, the receiver operating characteristic (ROC) and area under the curve (AUC) were used to assess the diagnostic values of the miRNAs to discriminate cancerous from non-cancerous states of the samples.The expression levels of miR-30c, miR-144, miR-375, miR-214, and miR-195 in CRC tissue were significantly downregulated (all P < .05; Paired T-Test) than that in normal adjacent tissue sample (NATS), while the expression of miR-141, miR-182, miR-183, miR-21, and miR-370 in CRC tissue were significantly upregulated (all P < .001) than that in NATS.
Most patients with advanced colorectal cancer (CRC) eventually develop resistance to systemic combination therapy. miR-195-5p and miR-497-5p are downregulated in CRC tissues and associated with drug resistance.
Finally, to assess the effects of miR-195-5p on GDPD5 levels and CRC cell chemoresistance, we generated luciferase reporter plasmids with either the wild-type 3'UTR miR-195-5p potential binding sites or mutant binding sites of GDPD5.
The 3' UTR of Notch signaling proteins Notch2 and RBPJ, which are essential genes in CRC cell stemness and chemoresistance, possessed double putative binding sites of miR-195-5p. qRT-PCR and western blot assays demonstrated significant decreases in Notch2 and RBPJ when CRC cell lines were exposed to miR-195-5p and significant increases when exposed to anti-miR-195-5p.
Using bioinformatics-based prediction and luciferase reporter system, we found that coactivator-associated arginine methyltransferase 1 is post-transcriptionally targeted by microRNA-195-5p in colorectal cancer.
Aberrant expression of miR-195 has been found to be involved in colorectal cancer (CRC); however, its function and underlying mechanism in the radioresistance of CRC remains unclear.
Using a miR real-time quantitative polymerase chain reaction (RT-qPCR), we observed that expression levels of miR-93, miR-195, and let-7b were significantly decreased, whereas those of miR-7, miR-141 and miR-494 showed increases that were more significant in the CRC tissue samples from the early relapsed patients than in those from the non-early relapsed patients.
Furthermore, miR-17-5p (p = 0.011) and miR-20a-5p (p = 0.003) were up-regulated expression in the III/IV tumor stage, miR-145-5p (p = 0.028) and miR-195-5p (p = 0.001) were significantly increased expression with microscopic vascular invasion in CRC tissues, miR-17-5p (p = 0.037) and miR-145-5p (p = 0.023) were significantly increased expression with lymphovascular invasion.
The 15 differentially expressed miRNAs, especially hsa-miR-195 and hsa-miR-20a may be used as potential biomarkers for early detection and screening of colorectal cancer.
Similarly to miR-195, the members of the same miR family, miR-424 that was upregulated, and miR-15a, miR-15b and miR-16 that were unaltered in expression in CRC tissues compared with paired adjacent normal mucosa, did not appear to have a role in regulating the expression of IGF1-R. Taken together, these results identify downregulation of miR-497 as an important mechanism of upregulation of IGF1-R in CRC cells that contributes to malignancy of CRC.
Here, we assess miR-195 expression in colorectal cancer, which has not been investigated before, and its clinical significance including survival analysis.
Moreover, introduction of miR-195 dramatically suppressed the ability of HCC and colorectal carcinoma cells to form colonies in vitro and to develop tumors in nude mice.