The expression levels of miR31, miR92a, KRAS oncogene, and the c-MYC transcription factor were subexpressed upon 72 h post-treatment with kaempferol-3-<i>O</i>-glycoside compared with the control without treatment (<i>P</i> < .05); in contrast, the tumor suppressor genes AMPK (∼4.85, <i>P</i> = .005) and APC (∼2.71, <i>P</i> = .066) tumor suppressors genes were overexpressed.
Therefore, it is necessary to explore its pathogenesis and identify some reliable prognostic biomarker of RCC. miRNAs are emerging as important players in the development and progression of RCC. miR-31-5p has been reported to act as a tumor suppressor in hepatocellular carcinoma (HCC).
This, together with clinical data analysis, revealed that the expression of miR-31 was associated with tumor differentiation, metastasis, and staging of patients, and the survival period of patients with lowly expressed miR-31 was longer.
Furthermore, low expression of miR-31-5p was highly correlated with tumor-node-metastasis (TNM) stage (I+II vs III+IV, p=0.001), T classification (T1 vs T2+T3+T4，p=0.036) and local lymph node metastasis (N1-N3 vs N0, p=0.002), but not distant metastasis (p=0.288).
The expression levels of miR-27a and miR-31 are related to distant metastasis and tumor grade of patients with colorectal cancer, and positively associated with the survival time of patients, having high diagnostic value.
Furthermore, low expression of miR-31-5p was highly correlated with tumor-node-metastasis (TNM) stage (I+II vs III+IV, p=0.001), T classification (T1 vs T2+T3+T4, p=0.036) and local lymph node metastasis (N1-N3 vs N0, p=0.002), but not distant metastasis (p=0.288).
The expression levels of microRNA‑31 (miR‑31) and LOC554202 have been previously investigated in colorectal cancer (CRC) and their oncogenic and/or tumor suppressive roles have been described.
Overall, our data suggest that the loss of miR-31-5p from HCC tumors promotes chemosensitivity, and this knowledge may be prognostically beneficial in the context of therapeutic sensitivity.
MiR-31 is a representative example as it can not only enhance tumor development and progression in pancreatic cancer, colorectal cancer and so on, but also inhibit tumorigenesis and induce apoptosis in ovarian cancer, prostate cancer and etc.
In conclusion, detection of miR-21, miR-135b, miR-31 and miR-20a levels in the tissue might be helpful to illuminate the molecular mechanisms underlying CRC carcinogenesis and serve as tumor-associated biomarkers for diagnosis.
Previously, we determined microRNA-31 (miR-31) is a noncoding tumor suppressive gene frequently deleted in glioblastoma (GBM); miR-31 suppresses tumor growth, in part, by limiting the activity of NF-κB.
This system was fabricated by conjugation of microRNA-31 onto doxorubicin-loaded mesoporous silica nanoparticles with a poly(ethyleneimine)/hyaluronic acid coating, and drug release was triggered by acidic environment of tumors.
Herein, we describe small-molecule inhibitors of miR-31, a tumor-associated microRNA (miRNA), identified by high-throughput screening using a cell-based reporter assay.
Our data showed that overexpression of miR-31 induced markedly inhibition of HCC cell proliferation, migration in vitro and inhibited xenograft tumor growth in vivo.
However, it remains to be evaluated whether this system can be applied for tumor miRNA therapy. miR-31-5p, a tumor suppressive miRNA involved in the tumorigenesis of EBV-positive NPC, was selected as the therapeutic miRNA to be transferred.
Furthermore, the results revealed that miR-31 promoted proliferation and EMT in cervical cancer cells and accelerated the development of tumor growth <i>in vivo</i> xenograft experiment by inhibiting BAP1 expression.