| Literature DB >> 33260155 |
Fei Geng1, Gui-Feng Lu2, Yu-Jun Luo3, Sky Dominguez4, De-Ying Kong1, Lian-Hua Shen2, Xiao-Mei Luo1, Xin Yang1, Min Hu1, Wen-Shan Lai1, Zhi-Shui Jiang1, Yuan-Shou Chen1.
Abstract
Glioma is a primary, malignant, and aggressive brain tumor in adults. To develop new therapeutic strategies for glioma, we must determine its underlying mechanisms. In the present study, we aimed to investigate the potential role of miR-1272-ADAM9-CDCP1 signaling in the progression of glioma. We found that ectopic expression of miR-1272 produced significant inhibitory effects on cell proliferation and migration and was associated with cell cycle G0/G1 arrest in A172 and SHG44 glioma cells. Using the luciferase reporter assay, we identified ADAM9 as a target of miR-1272. The expression of ADAM9 was markedly decreased or increased after overexpression or inhibition, respectively, of miR-1272 in glioma cells. Moreover, overexpression of ADAM9 reversed the inhibitory effects of miR-1272 on glioma cell progression. Furthermore, CDCP1 served as a potential downstream molecule of miR-1272/ADAM9 signaling in glioma and promoted the proliferation and migration of glioma. Results derived from clinical samples and online databases confirmed correlations between the expression of ADAM9 and CDCP1 and both the severity and prognosis of glioma. In conclusion, these results suggest that miR-1272 and CDCP1 may act as novel regulators in glioma. The miR-1272/ADAM9/CDCP1 pathway may serve as a potential candidate pathway for the prevention of glioma.Entities:
Keywords: ADAM9; CDCP1; glioma; miR-1272
Mesh:
Substances:
Year: 2020 PMID: 33260155 PMCID: PMC7835014 DOI: 10.18632/aging.202196
Source DB: PubMed Journal: Aging (Albany NY) ISSN: 1945-4589 Impact factor: 5.682