All these results demonstrated that Emodin inhibited tumorigenesis in liver cancer by simultaneously inhibiting the VEGFR<sub>2</sub>-AKT-ERK<sub>1/2</sub>signaling pathway and promoting a miR-34a-mediated signaling pathway.
Colorectal cancer (CRC) is a major cause of cancer-related deaths worldwide. miR-34 induces changes of its downstream genes and plays a key role in altering the apoptotic cycle and pathways of downstream cells and therefore influences carcinogenesis.
Taken together, our findings support a model in which the KLF5, MYC/LINC00346/miR-34a-5p cross-talk served as critical effectors in GC tumorigenesis and progression, suggesting a new therapeutic direction in the treatment of GC.
MiR-34a is involves in certain epithelial-mesenchymal transition (EMT)-associated signal pathways to repress tumorigenesis, cancer progression, and metastasis.
Moreover, miR‑34 has been identified as a tumour‑suppressor in GC. p53‑induced miR‑34 regulates several different target genes and signalling pathways, inducing apoptosis, senescence, and cell cycle arrest and repressing GC cell proliferation, migration and metastasis, thus contributing to the suppression of carcinogenesis and GC cancer progression.
We concluded MiR-34a-5p suppressed tumorigenesis and progression of glioma and potentiated TMZ-induced cytotoxicity for glioma cells by targeting HMGA2, deepening our understanding on molecular basis of HMGA2 in glioma.
Therefore, we hypothesized that the individual miR-34 family members, which are tumor suppressive miRNAs, would have varying effects on lung tumorigenesis.
The miR-34 family of microRNAs suppresses the expression of proteins involved in pluripotency and oncogenesis. miR-34 expression is frequently reduced in cancers; however, the regulation of their expression is not well understood.
Our findings suggest that functional loss or suppression of the tumor suppressor CXCL10 due to induction of miR-34a leads to inhibition of the TLR signaling pathway during breast tumorigenesis, providing a novel target for the molecular treatment of breast malignancies.
We find that miR-34a suppresses breast carcinogenesis, at least in part by lowering the levels of tRNA<sub>i</sub><sup>Met</sup> through AGO2-mediated repression, consequently inhibiting the proliferation of breast cancer cells and inducing cell cycle arrest and apoptosis.
Mice with disruption of Mir34a and/or Tp53 specifically in intestinal epithelial cells (IECs) (Mir34a<sup>ΔIEC</sup> mice, Tp53<sup>ΔIEC</sup> mice, and Mir34a<sup>ΔIEC</sup>/Tp53<sup>ΔIEC</sup> mice) and controls (Mir34a<sup>Fl/Fl</sup>/Tp53<sup>Fl/Fl</sup>) were given azoxymethane to induce colorectal carcinogenesis.
The natural language processing (NLP), gene ontology (GO), pathway and network analyses were performed to analyze the genes associated with the carcinogenesis and progression of HCC and the targets of miR-34a predicted in silico.
MicroRNAs (miRNAs) are a large family of small, non-coding RNAs that play a pivotal role in tumorigenesis. miR‑34a, which is a member of the miR-34 family, is a downstream target of p53.
These findings suggest that miR-34 and miR-124 loci methylation could be a tumor-associated frequent event during NSCLC tumorigenesis and could be used as powerful markers for the prognosis of patients with NSCLC.