Disrupting the Pairing Between let-7 and Hmga2 Enhances Oncogenic Transformation | Zendy

Christine Mayr | Zendy; Michael T. Hemann | Zendy; David P. Bartel | Zendy

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Disrupting the Pairing Between let-7 and Hmga2 Enhances Oncogenic Transformation

Author(s) -

Christine Mayr,

Michael T. Hemann,

David P. Bartel

Publication year - 2007

Publication title -

science

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 12.556

H-Index - 1186

eISSN - 1095-9203

pISSN - 0036-8075

DOI - 10.1126/science.1137999

Subject(s) - psychological repression , microrna , carcinogenesis , biology , hmga2 , transformation (genetics) , genetics , oncogene , phenotype , oncomir , chromosomal translocation , microbiology and biotechnology , gene , gene expression , cell cycle

MicroRNAs (miRNAs) are approximately 22-nucleotide RNAs that can pair to sites within messenger RNAs to specify posttranscriptional repression of these messages. Aberrant miRNA expression can contribute to tumorigenesis, but which of the many miRNA-target relationships are relevant to this process has been unclear. Here, we report that chromosomal translocations previously associated with human tumors disrupt repression of High Mobility Group A2 (Hmga2) by let-7 miRNA. This disrupted repression promotes anchorage-independent growth, a characteristic of oncogenic transformation. Thus, losing miRNA-directed repression of an oncogene provides a mechanism for tumorigenesis, and disrupting a single miRNA-target interaction can produce an observable phenotype in mammalian cells.

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