miR-424 expression

However, the effects of miR-424 inhibitor were markedly reversed by sh-PTEN. This study provides a potential novel therapeutic strategy for the prevention and treatment of EC by targeting miR-424.

This miRNA is also involved in the regulation of E2F transcription factors. The current review aims at summarization of the role of miR-424 in the process of cancer evolution and its impact on clinical outcome of patients in order to find appropriate markers for malignancies.

The inhibition rates of sorafenib on HepG2 cells in the mimic+OE-KIF23 group and the OE-KIF23 group were 47.491%±3.863% and 36.246%±6.063% (t=3.027, P<0.05). miR-424-5p can inhibit the proliferation, migration and invasion of HCC cells and can increase the sensitivity of HCC cells to sorafenib by targeting the expression level of KIF23.

The majority of patients (88.9%) received intensive treatment: DA-60 (daunorubicin 60mg/m2 + cytarabine 200mg/m2) regimen (50%), followed by DAC (DA-60 + cladribine 5mg/m2) (40%) and DA-90 (daunorubicin 90mg/m2 + cytarabine 100mg/m2) (10%). Azacitidine in standard dose was used as the low-intensity regimen...These data indicate that miR-199-5p may be a potential prognostic factor in AML patients. Larger studies are needed to confirm our observation.

Additionally, combined treatment with atorvastatin and carboplatin synergistically reduced tumor growth, chemoresistance, and peritoneal seeding in the intraperitoneal mouse models of ovarian cancer. We identified a novel NANOG-miR-424/503-WEE1 pathway for regulating ovarian CSCs, which has potential therapeutic utility in ovarian cancer treatment.

The results demonstrate that the expression of P53 protein has a high predictive value for predicting the occurrence of BRAIN metastases in NSCLC patients. Also, the high expression of miR-424 suggests that it is closely related to the occurrence of platinum resistance in NSCLC patients.

circ_0004872 suppresses the proliferation, invasion, and glycolysis of OSCC cells by sponged miR-424-5p, and promotes apoptosis, which can be used as a potential target for early diagnosis and targeted therapy of OSCC.

miR-424-5p was a target gene of circCBFB, and miR-424-5p negatively mediated ATG14. CircCBFB inhibits miR-424-5p and upregulates ATG14, thus promoting HCC cell proliferation and autophagy.

Furthermore, overexpression of miR-424 regulated the expression of PDCD4, Bax, Bcl-2, phosphorylated-PI3K/AKT and caspase-3, which was restored after co-transfection with pcDNA3.1-PDCD4. Collectively, the results indicated that miR-424 regulated the progression of cerebral ischemic stroke in a cellular model by targeting PDCD4.

Addition of the demethylating agent significantly reduced cell proliferation, migration, invasion, and OGT expression, while significantly increasing the expression of miR-424-5p. Altogether, these findings suggest that epigenetic downregulation of miR-424-5p, which in turn augments OGT expression, contributes to the creation of aggressive forms of stage I ccRCC.

However, these effects were partially neutralized by miR-424-5p inhibitors. LINC00922 increases the cell viability, migration, invasion and EMT process of HCC cells by regulating the miR-424-5p/ARK5 axis, and thus may serve as a potential target for targeted therapy.

MiR-424 inhibits HCC cell autophagy and proliferation through regulating ATG14.

ROC curve analysis manifested an area under the curve of 0.768 with a sensitivity of 75.0% and a specificity of 72.4%, suggesting that serum miR-424 had high diagnostic value in HCC patients. The data suggest that serum miR-424 may represent a biomarker in early detection of HCC.

LINC00641 inhibits the development of CSCC by downregulating miR-424.

miR-424-5p silencing and FGF2 overexpression both reversed the suppressive effects of SNHG1 knockdown on the proliferation, migration and invasion of OS cells. Thus, the silencing of SNHG1 may inhibit the proliferation, migration and invasion of OS cells by regulating the miR-424-5p/FGF2 axis.

The present study suggests that hypermethylation downregulates miR-424. VEGF expression is upregulated with decreased miR-424 in colorectal cancer, which results in cancer progression.

Collectively, our findings indicate that MSC-derived EVs transfer miR-424 to down-regulate MYB, which ultimately led to the inhibition of the tumorigenesis and angiogenesis of ovarian cancer. Hence, this study offers a potential prognostic marker and a therapeutic target for ovarian cancer.

In summary, the immune landscape with abnormal infiltration of macrophages may be one of the prelude to the cancerous process. The novel macrophages-related 4-gene signature is expected to become a potential prognostic marker in liver cancer.

Our results proved that E2F7 was a direct target of miR-424-5p, and miR-424-5p could regulate cell cycle and further inhibit the proliferation of HCC cells by targeting E2F7.

MiR-424-5p could be considered as a potential tumor-suppressor miR in regulating BC cellular growth, apoptosis, and T cell-related immune response through targeting PD-L1, and its downstream mediators. Therefore, we recognized miR-424-5p as a promising candidate for miR restoration therapy in BC patients.

Transfection of miR-424-3p mimics could significantly reduce the regulatory effect of ethyl acetate extract of peony seed coat on CAL27 cell proliferation, apoptosis and STAT3/Survivin pathway. It concluded that ethyl acetate extract of peony seed coat could inhibit the activation of the STAT3/Survivin signaling pathway by down-regulating the expression of miR-424-3p, thereby inhibiting the proliferation of oral squamous carcinoma cells and inducing apoptosis.

Furthermore, it suppresses tumor angiogenesis, modulating surrounding endothelial cell proliferation and migration as well as the morphology of blood vessels, and angiogenic growth factors. These findings suggest that melatonin could play a pivotal role in tumor suppression via miR-424-5p/VEGFA axis.

KEGG signaling pathway analysis indicated that the DEGs were significantly enriched in 'endocytosis', 'regulation of actin cytoskeleton', 'Wnt signaling pathway' and 'ubiquitin-mediated proteolysis signaling pathway'. These results suggested that miR-424-5p is a potential target in the treatment of CRC.