TY - JOUR
T1 - MicroRNAs/TP53 feedback circuitry in glioblastoma multiforme
AU - Suh, Sung Suk
AU - Yoo, Ji Young
AU - Nuovo, Gerard J.
AU - Jeon, Young Jun
AU - Kim, Seokho
AU - Lee, Tae Jin
AU - Kim, Taewan
AU - Bakac̀s, Arianna
AU - Alder, Hansjuerg
AU - Kaur, Balveen
AU - Aqeilan, Rami I.
AU - Pichiorri, Flavia
AU - Croce, Carlo M.
PY - 2012/4/3
Y1 - 2012/4/3
N2 - MicroRNAs (miRNAs) are increasingly implicated in regulating cancer initiation and progression. In this study, two miRNAs, miR-25 and -32, are identified as p53-repressed miRNAs by p53-dependent negative regulation of their transcriptional regulators, E2F1 and MYC. 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.
AB - MicroRNAs (miRNAs) are increasingly implicated in regulating cancer initiation and progression. In this study, two miRNAs, miR-25 and -32, are identified as p53-repressed miRNAs by p53-dependent negative regulation of their transcriptional regulators, E2F1 and MYC. 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.
UR - http://www.scopus.com/inward/record.url?scp=84859470540&partnerID=8YFLogxK
U2 - https://doi.org/10.1073/pnas.1202465109
DO - https://doi.org/10.1073/pnas.1202465109
M3 - مقالة
C2 - 22431589
SN - 0027-8424
VL - 109
SP - 5316
EP - 5321
JO - Proceedings of the National Academy of Sciences of the United States of America
JF - Proceedings of the National Academy of Sciences of the United States of America
IS - 14
ER -