Our findings suggest that c-Myb is an evolutionally conserved target of miR-150 and miR-150/c-Myb interaction is important for embryonic development and possibly oncogenesis.
Only one miR-150 was found to show a decrease in expression levels in the three tissue groups (normal, adenoma and cancer tissue) in parallel with increasing carcinogenesis of the colorectal tissue.
Reduced miR-150 and miR-3940-5p expression in tumor tissues and embryonic lung tissues suggests that these miRs may be involved in the tumorigenesis or de-differentiation of NSCLC.
Tumor protein p53, a transcriptional factor, plays an important role in the progression of tumorigenesis. miR-150 was the only miRNA predicted to target 3'-UTR of p53 by Targetscan.
MiR-150, a member of small non-coding RNAs, has been proven to dysregulate in different types of tumor and bear on carcinogenesis and cancer prognosis by regulating the expression of a series of gene including utrophin.
The present results suggest that miR-150 is overexpressed in HPV-induced lesions in this model and its expression seems to increase with lesion progression, along the process of multi-step carcinogenesis.
Upregulation of miR‑150 suppresses nasopharyngeal carcinoma (NPC) cell proliferation and induces G1/S arrest in vitro, and inhibits tumorigenesis in vivo.
Microenvironmental microRNAs (miRNAs) such as miRNA-146a and miRNA-150 regulate cancer-associated inflammation and are involved in HPV-induced carcinogenesis.
As an example, the results showed that miR-150-5p downregulated the CCR2 expression in monocytes by targeting Notch 3, thus leading to the suppression of tumorigenesis.
The purpose of this study was to further investigate the potential role of miR-150-5p in the progress of cervical carcinoma cells including proliferation and epithelial-mesenchymal transition (EMT).The ability of miR-150-5p to promote carcinogenesis was analyzed using quantitative reverse transcription polymerase chain reaction (qRT-PCR) and western blot assays, respectively.