The enhanced expression of miR-31 has been observed in many human malignancies including lung cancer, and this microRNA regulates several aspects of oncogenesis.
Following the cloning of miR-31 and miR-143 into vectors, their expressions were determined before treatment with constructs of miR-31 and miR-143 in cancer cell lines and normal breast cells.
Interestingly, MIR31HG/miR-31 could not regulate each other's expression in certain cancer, suggesting that the role of MIR31HG in cancer is independent of miR-31.
Importantly, we reveal a novel drug-resistance mechanism in which the transcription factor FOXC1 binds to the miR-31 promoter to increase the expression of miR31-5p and regulate LATS2 expression, resulting in cancer cell resistance to OXA.
Meanwhile, WIR (25 mg/kg) restored the miR-31-5p level which was up-regulated in the CAC model group, and ectopic expressions of the miR-31-5p down-stream LATS2 and YAP genes in the hippo pathway were also modulated by the WIR (25 mg/kg) treatment.
Within the top five of the miRNAs screened, we validated miRNA-31 (miR-31) and miR-135b as up-regulated, while miR-193a-3p was down-regulated in BRAF-mutated cancer.
The polycomb group protein enhancer of zeste homolog 2 (EZH2) is a methyltransferase that suppresses microRNA-31 (miR-31) in various human malignancies including colorectal cancer.
Although aberrant expression of miR-31 has been found in different types of cancer, its pathophysiological effect and role in tumorigenesis still remain to be elucidated.
Significant upregulation of mir31 and downregulation of its target gene, CXCL12, in cancer, LK and LP tissues suggest their importance in progression of precancer to cancer.
These results suggest that miR-31 might inhibit the growth of lung adenocarcinoma cancer stem-like cells via down regulation of the MET-PI3K-Akt signaling pathway.
Here, we form four major conclusions regarding the role of these proteins in CRC and their potential clinical value: (i) SATB2 is a sensitive marker to distinguish CRC from other cancer types, (ii) Reduced expression of SATB2 in CRC is associated with poor prognosis, (iii) High levels of SATB1 expression facilitate CRC and are associated with poor prognosis and (iv) Overexpression of miR-31 and -182 in CRC leads to more aggressive cancer.
Overall, we suggest that miR-31 functions as a tumor suppressor by selectively regulating cell cycle and EMT regulatory proteins in human hepatocarcinogenesis providing a novel target for the molecular treatment of liver malignancies.
Expression of hsa-miR-31 was significantly up-regulated in both cancer and leukoplakia tissues and, thus, may be one of the molecular markers of leukoplakia which may progress to gingivo-buccal cancer.
Data were extracted from studies comparing overall survival (OS), cancer-specific survival (CSS), or postoperative survival (PS) in patients with multiple cancers, which showed higher miR-31 expression than with similar patients.
Alterations of miRNAs expression in cancer tissue may be reflected in circulation.We attempted to investigate the expression and clinical significance of plasma miR-20a, miR-31 and miR-375 in patients with non-small cell lung cancer (NSCLC).