Furthermore, mutant ACTB mRNA 3'-UTR promoted hepatocellular carcinoma cells migration and invasion in vitro and in vivo by up-regulating miR-1 target gene MET and miR-29a target gene MCL1.
Moreover, SOCS1 overexpression reverses the activity of SOCS1/STAT6 signals of macrophages and cell proliferation and invasion of OSCCs induced by miR-29a-3p overexpression.
Moreover, miR-29a promoted cell apoptosis, suppressed proliferation, inhibited migration and invasion via inactivation of NF-κB signaling pathway in cervical cancer cells.
In conclusion, miR‑29a promoted the apoptosis, and inhibited the invasion, migration and EMT process of OS cells via inhibition of the SOCS1/NF‑κB signalling pathway by directly targeting DNMT3B.
In addition, miR-29a robustly promotes invasion in PTEN-deficient glioblastoma cells by repressing translation of the Sox4 transcription factor, and this upregulates the invasion-promoting protein, HIC5.
Correction: miR-29a contributes to breast cancer cells epithelial-mesenchymal transition, migration, and invasion via downregulating histone H4K20 trimethylation through directly targeting SUV420H2.
MiR-29a inhibited cell proliferation, migration, and invasion, as well as promoted cell apoptosis through repressing the PAK1/LIMK signaling pathway by targeting CDC42 in cervical cancer.
After transfection and stimulation with SEVO, biological activities of Huh7 and HepG2 cells were evaluated using the cell counting kit-8, Annexin V-fluorescein isothiocyanate apoptosis detection kit, 24-well cell migration assay kit, and tumor invasion 24-well plates. miR-29a and protein expression were quantified with quantitative reverse transcription polymerase chain reaction and Western blot assay, respectively.
Reintroduction of STAT3 without 3'‑untranslated region (3'UTR) reversed the inhibitory effects of miR‑29a on cell proliferation, migration and invasion.
We determined that IFITM3 was upregulated and miR‑29a downregulated in HCC tissues and that they were associated with HCC tumor size, tumor multifocal, and venous invasion.
Overexpression of miR-29a in GSCs inhibited expression of WTAP and suppressed both phosphoinositide 3-kinase/AKT and extracellular signal-related kinase pathways by downregulating QKI-6, thereby inhibiting cell proliferation, migration, and invasion but promoting apoptosis.
These results have provided us with information regarding the molecular mechanisms by which hyperinsulinemia promotes breast cancer occurrence and development and thus leads to a poor prognosis in breast cancer patients and indicate that miR-29a plays an important role in breast cancer development and invasion.
Two distinct subgroups of grade I-IV glioma patients with different prognoses were identified according to miR-29a/b/c expressions. miR-29a/b/c overexpressions suppressed glioma cell migration and invasion through targeting CDC42 and subsequently decreasing phosphorylated PAK1/2/3, LIMK1/2 and cofilin, the pivotal downstream effectors of CDC42.