miR-34a overexpression

In addition, the effect of LINRIS overexpression was reversed by miR-34a overexpression. Therefore, LINRIS siRNA silencing in GC may promote cell apoptosis by promoting miR-34a maturation.

Overexpression of miR-34a-5p or silencing of FOXP1 reversed the protective effects of METTL14 silencing on cell injury in the PE model. In conclusion, METTL14 mediated m6A modification to promote miR-34a-5p expression, leading to the inhibition of FOXP1 expression, which aggravated endothelial cell damage in the PE cell model.

Oxaliplatin inhibits tumor growth, invasion, and metastasis by upregulating miR-34a, activating the expression of the upstream P53 gene, and driving the downregulation of survivin (P53/miR-34a/survivin axis) in BGC-823 gastric cancer cells.

Our findings highlight the significance of the miR-34a/Axl/Akt/GSK-3β signaling axis in modulating the malignancy of oral cancer cells. Targeting miR-34a may hold therapeutic potential in oral cancer treatment, as manipulating its expression can attenuate the aggressive behavior of oral cancer cells via the Axl/Akt/GSK-3β pathway.

The overexpression of miR-34a-5p or inhibition of SIDT2 expression negated the alleviative effects of METTL14 silencing on mitochondrial homeostasis imbalance. In conclusion, METTL14, through m6A modification, modulates the miR-34a-5p/SIDT2 axis, impairing mitochondrial homeostasis in NAFLD.

While these two neuroblastoma cell lines are phenotypically diverse and gene expression differences between them are extensive, we observed that the regulation of gene expression in both cell lines is in a stable equilibrium at early timepoints after exposure to ionizing radiation.

Inhibition of miR-34a transiently led to upregulation of FOXP1 mRNA expression and increased cellular invasion in vitro. Our data indicate that miR-34a could be a potential biomarker for improving the diagnostic efficiency of OC, and miR-34a overexpression may reduce OC pathogenesis by targeting FOXP1.

Through various immune cells, factors, and other mechanisms, miR-34a can inhibit tumor carcinogenesis. In view of the important role of miR-34a in tumors, this research reviewed the aspects of miR-34a regulation of tumor immune microenvironment to exert anti-tumor effects in order to clarify the potential immunotherapy value of miR-34a in tumors.

JMJD2A promoted docetaxel resistance in prostate cancer cells by regulating cytoskeleton remodeling through the miR-34a/STMN1/β3-Tubulin axis.

Cell viability and colony formation assays revealed that overexpression of miR‑34a in BC cells enhances the chemosensitivity of cisplatin, doxorubicin, epirubicin and mitomycin C. Furthermore, miR‑34a inhibited cell proliferation and triggered G0/G1 cell cycle arrest by inhibiting cyclin D1 and cyclin E2 protein expression. Moreover, miR‑34a suppressed cell motility through the downregulation of epithelial‑mesenchymal transition. In summary, miR‑34a inhibits cell proliferation, motility and autophagy activity in BC, which can benefit BC treatment.

The P53/miR-34a/SIRT1 positive feedback loop plays an important role in the termination of LR. Our findings showed the molecular and metabolic mechanisms of LR termination and provide a potential therapeutic alternative for treating P53-wild-type HCC patients.

MCM3AP-AS1 may enhance cell invasion, migration, and tumor formation capacity by regulating miR-34a in NSCLC cells.

Repression of the miR-34a-5p-c-MYC-CHK1/CHK2 axis contributes to the acquisition of radioresistance in HCC cells. In summary, the miR-34a-5p-c-MYC-CHK1/CHK2 axis counteracts cancer stem cell-like properties and enhances radiosensitivity in hepatocellular cancer through repression of the DNA damage response.

The cell death rate was 6%, 9% and 12% in U87, 13%, 21% and 40% in U87EGFRvIII cells for CDA, miR-34a and CDAmiR treatment respectively, showing a higher apoptosis rate in the cells receiving both drugs compared to when single therapy was applied. The experimental findings clearly show the improved apoptosis rate of GBM cells when treated by engineered exosomes armed with two gene therapy agents and targeted toward EGFRvIII antigen.

An apoptosis assay of prostate cancer cells (PRAD) confirmed that the overexpression of miR-34a-5p inhibited paclitaxel-induced apoptosis and promoted cell proliferation...Moreover, the Western blotting (WB) and quantitative PCR (qPCR) assays demonstrated that the overexpression of miR-34a-5p induced down-regulation of the SIRT-related proteins HIF2α and PGC1α, while on the contrary, it up-regulated the expression of two tumour suppressor genes, TP53 and VEGF. In conclusion, we have shown that miR-34a-5p is involved in the oncogenesis of PRAD cells via the SIRT1/TP53 axis.

Luciferase reporter assay indicated that DOCK8 was a direct target gene of miR-34a. These data indicates miR-34a may induce neutrophil apoptosis by regulating Cdc42-WASP-Arp2/3 pathway-mediated F-actin remodeling and ROS production.

The autophagy inhibitors chloroquine (CQ) and bafilomycin A1 (Baf-A1) increased PD-L1 expression in BC cells through the ERK-JNK-c-Jun signal-transduction pathway...Our results provide evidence that autophagy blockade and its regulatory pathway affect cancer-associated immunosuppression through PD-L1 elevation. Thus, the coadministration of autophagy inhibitors and a PD-L1 immune checkpoint blockade provides a potential therapeutic approach for treating BC.

Cell proliferation analysis showed that overexpression of circCTNNA1 reversed the inhibitory effects of overexpression of miR-34a on cell proliferation. Upregulation of circCTNNA1 in MCL predicts poor survival of patients and it may sponge miR-34a to promote cancer cell proliferation.

Therefore, AK077216 may inhibit CRA cell migration and invasion by downregulating miR-34a.

Therefore, OIP5-AS1 was upregulated to enhance the expression of oncogenic PD-L1 by sponging miR-34a in NSCLC, leading to promoted NSCLC cell proliferation. Our study also demonstrated that OIP5-AS1 was upregulated while miR-34a was downregulated in NSCLC.

In addition, overexpression of miR-34a enhanced the effects of overexpression of WTAPP1 and EEF2K on apoptosis. WTAPP1 may promote TNBC cell proliferation by downregulating miR-34a.

Crocin promoted apoptosis and increased caspase-3 activity and LDH release, which were reversed by ROS scavenger N-acetyl-L-cysteine (NAC), miR-34a overexpression, and PTPN4 silencing. To conclude, crocin promoted ROS-mediated apoptosis of PTC cells by modulating the miR-34a-5p/PTPN4 axis.

Our findings thus show a significant role of KLF4 in tumorigenesis and TAM polarization of NSCLC. However, miR-34a-5p mediated targeting of these molecular networks will provide a better therapeutic intervention for NSCLC.

miR-34a-5p mediates growth, migration and other malignant behaviors in CC by regulating CDC25A.

Restoring miR-34a-5p or depleting c-MYC in MSC-EV limited CRC tumor formation. MSC-EV-derived miR-34a-5p depresses CRC development through modulating the binding of c-MYC to DNMT3a and epigenetically regulating PTEN.

Moreover, miR-34a overexpression reduced the enchaining effects of prominin 1 on LC cell proliferation. Therefore, miR-34a might suppress LC cell proliferation by targeting prominin 1.

Overall, these results demonstrated that REV exerts anti-cancer effects on OC cells through an miR-34a/Bcl-2 axis, highlighting the therapeutic potential of REV for treatment of OC.

Moreover, miR-34a overexpression inhibited ZEB1 expression and melanoma tumor growth in vivo, in a melanoma nude mouse model. Together, these findings demonstrate that miR-34a inhibits melanoma growth by targeting the proto-oncogene ZEB1 and suggest the miR-34a -ZEB1 axis may serve as a novel target for melanoma treatment.

In addition, overexpressed miR-34a downregulated the expression of its target genes. Taken together, our results demonstrated, for the first time, the potential of rAAV-mediated efficient modulation of miR-34a expression in the prostate to inhibit PCa progression by regulating its downstream gene expression.

The long non-coding RNA (lncRNA) imatinib-upregulated (IUR) has been recently reported as a tumor suppressor in leukemia...However, CD44 overexpression played an opposite role and attenuated the effects of IUR and miR-34a overexpression. In conclusion, the results from this study demonstrated that IUR may upregulate miR-34a expression in order to inhibit PAAD cell migration and invasion by downregulating CD44.