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However, miR-25 and -32 result in p53 accumulation by directly targeting Mdm2 and TSC1, which are negative regulators of p53 and the mTOR (mammalian target of rapamycin) pathway, respectively, leading to inhibition of cellular proliferation through cell cycle arrest. Thus, there is a recurrent autoregulatory circuit involving expression of p53, E2F1, and MYC to regulate the expression of miR-25 and -32, which are miRNAs that, in turn, control p53 accumulation. Significantly, overexpression of transfected miR-25 and -32 in glioblastoma multiforme cells inhibited growth of the glioblastoma multiforme cells in mouse brain in vivo. The results define miR-25 and -32 as positive regulators of p53, underscoring their role in tumorigenesis in glioblastoma.<\/jats:p>","DOI":"10.1073\/pnas.1202465109","type":"journal-article","created":{"date-parts":[[2012,3,20]],"date-time":"2012-03-20T00:57:11Z","timestamp":1332205031000},"page":"5316-5321","update-policy":"https:\/\/doi.org\/10.1073\/pnas.cm10313","source":"Crossref","is-referenced-by-count":120,"title":["MicroRNAs\/TP53 feedback circuitry in glioblastoma multiforme"],"prefix":"10.1073","volume":"109","author":[{"given":"Sung-Suk","family":"Suh","sequence":"first","affiliation":[{"name":"Department of Molecular Virology, Immunology, and Medical Genetics, Comprehensive Cancer Center, Ohio State University, Columbus, OH 43210;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ji Young","family":"Yoo","sequence":"additional","affiliation":[{"name":"Dardinger Laboratory for Neuro-Oncology and Neurosciences, Department of Neurological Surgery, 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