No significant changes in the expression of miR-31-3p were observed when sequential tissue biopsies were tested in long-term or poor responders to anti-EGFR mAbs. miR-31-3p scores were similar when pretreatment biopsies were compared with treatment-naïve archival tissues (often primary colorectal cancer).
In addition, as a sponge of miR-31, the low level of hsa_circ_0000523 led to activation of Wnt/β-catenin signaling pathway, inducing the subsequent progress of colorectal cancer.
In this study, we identified the host gene of mouse miR-31 and found that miR-31 was over-expressed in both human colorectal cancer and mouse colon cancer models.
In summary, miR-31 can inhibit autophagy in colorectal CAFs, affect colorectal cancer development, and increase the radiosensitivity of colorectal cancer cells co-cultured with CAF.
For example, in breast cancer loss of miR-31 expression is associated with high risk of metastases, whereas in colorectal cancer high miR-31 expression correlates with advanced disease stage.
Taken together, our results demonstrate for the first time that miR-31 plays a significant role in activating the RAS signaling pathway through the inhibition of RASA1 translation, thereby improving colorectal cancer cell growth and stimulating tumorigenesis.
We found that 67 miRNA precursors are upregulated in rectal cancer (p<0.05) and 21 of those have never been reported in colorectal cancer (CRC); 39 miRNA precursors are downregulated (p<0.05) and 24 novel dysregulated miRNAs were identified in rectal cancer. miR-31, miR-126 and miR-143 are differentially expressed between colon cancer and rectal cancer.