We observed significantly greater expression of <i>TLR4</i>, <i>IL1B</i>, <i>IL8</i>, and miR-135b in CRA lesions and <i>TLR2</i>, <i>IL1B</i>, <i>IL6</i>, <i>IL8</i>, miR-34a and miR-135b in CRC tumours compared to their respective normal tissues.
Suppression of these miRNAs implicated an inverse function, while altered expression of ST6GALNAC2 mediated CRC progression upon transfection with miR-135b/-182 mimic or inhibitor.
Accordingly, some of the overexpressed miRNAs especially the miR-135b-5p, -373-3p, 183-5p, 142-5p, 200c-3p, and 19a-3p may play key roles in CRC pathophysiology through MTUS1.
Taken together, our findings provide the first evidence supporting the role of miR-135b as an oncogene in CRC via the inhibition of TGFBR2 translation.
In stool samples, level of miR-135b was significantly higher in subjects with CRC (P < 0.0001) or adenomas (P < 0.0001), but not in patients with IBD compared with controls. miR-135b showed a significant increasing trend across the adenoma to cancer sequence (P < 0.0001).
In this study, we evaluated the role of miR-135b in colorectal cancer (CRC) and its regulatory role for metastasis suppressor-1 (MTSS1) and its mechanisms.
The 2 most upregulated (miR-31; miR-135b) and most downregulated (miR-1; miR-133a) miRNAs identified CRC in our "test" set with 100% sensitivity and 80% specificity.