The expression of HMGA genes is regulated by their 3′UTR

Borrmann, Lars; Wilkening, Stefan; Bullerdiek, Jörn

doi:10.1038/sj.onc.1204577

Cited by 70 publications

(59 citation statements)

References 31 publications

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“…3 In fact, the breakpoint, at the genomic level, was mapped within the 3 0 UTR of the gene, a region containing regulatory elements that exert posttranscriptional expression control. 4 It can be, therefore, hypothesized that the removal of this gene segment alters the expression pattern of HMGA2 by upregulation of the 'wild-type' transcript (HMGA2a) rather than by switching towards cryptic or aberrant splicing products. HMGA2 encodes a protein that belongs to the non-histone chromosomal high-mobility group protein A family (HMGA).…”

mentioning

confidence: 99%

t(3;12)(q26;q14) in polycythemia vera is associated with upregulation of the HMGA2 gene

Storlazzi

Albano

Locunsolo³

et al. 2006

Leukemia

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mentioning

confidence: 99%

t(3;12)(q26;q14) in polycythemia vera is associated with upregulation of the HMGA2 gene

Storlazzi

Albano

Locunsolo³

et al. 2006

Leukemia

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“…Clones were verified by sequencing. Cell culture of cell lines HeLa (cervix carcinoma), MCF7 (breast cancer), and L14tsv40 (lipoma, having a t(3; 12)(q27; q14) translocation involving HMGA2) as well as promoter assay experiments were performed as described elsewhere, with some minor modifications (Borrmann et al, 2001). Briefly, luciferase activities were measured after 48 h, and the experiments for each construct were performed in duplicate and repeated three times.…”

Section: Pcr Amplification Of Hmga2 Promoter Elementsmentioning

confidence: 99%

“…These results suggest that beyond a constitutive active promoter, there have to be negative regulatory elements that were not present in the 5 0 flanking regions analyzed so far controlling the HMGA2 expression. One of those regulatory elements could be located within the 3 0 UTR of HMGA2 because it was shown that HMGA2 expression depends on the length of the 3 0 UTR (Borrmann et al, 2001), suggesting expressional control at the post-transcriptional level.…”

Section: Introductionmentioning

confidence: 99%

Human HMGA2 promoter is coregulated by a polymorphic dinucleotide (TC)-repeat

et al. 2003

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HMGA proteins are thought to be causally involved in the progression of different diseases, including benign and malignant tumors, obesity, arteriosclerosis, and restenosis. As HMGA proteins are architectural transcription factors, their binding to DNA leads to changes in DNAconformation modulating the environment for the assembly and function of transcriptional complexes, thus influencing the expression of a huge variety of genes. Despite the emerging role of HMGA proteins for important diseases, only limited information is available about mechanisms regulating the expression of the HMGA2 gene. In this report, 2240 bp of the 5 0 flanking region of the HMGA2 gene were functionally analyzed by luciferase assay experiments. Besides the identification of novel positive and negative regulatory elements, it was shown that transcription is initiated from two independent promoter regions within cell lines HeLa, MCF7, and L14tsv40. Furthermore, a functional polymorphic dinucleotide repeat (TCTCT(TC) n ) 500 bp upstream of the ATG translational start codon was found to regulate strongly the human HMGA2 promoter with an activation pattern that correlates to its TC-repeat length.

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“…Interestingly, the post-transcriptional regulation of HMGA2 through its 3ЈUTR was originally implied 10 yr ago (Geurts et al 1997). It was shown that the HMGA2 transcript contains 10 ARE motifs (AUUUA) in its 3ЈUTR (Geurts et al 1997;Borrmann et al 2001). Borrmann et al (2001) performed reporter assays using several 3Ј deletion mutants of the HMGA2 mRNA, and showed that HMGA2 expression is negatively regulated by its 3ЈUTR.…”

mentioning

confidence: 99%

“…It was shown that the HMGA2 transcript contains 10 ARE motifs (AUUUA) in its 3ЈUTR (Geurts et al 1997;Borrmann et al 2001). Borrmann et al (2001) performed reporter assays using several 3Ј deletion mutants of the HMGA2 mRNA, and showed that HMGA2 expression is negatively regulated by its 3ЈUTR. Since they used a series of large truncations, it is not possible to say whether the effects of the deletion mutants reflect the loss of the let-7 targeting sites in the 3ЈUTR.…”

mentioning

confidence: 99%