The Tumor-Associated Gene HMGIC Is Expressed in Normal and Osteoarthritis-Affected Synovia

Broberg, Karin; Tallini, Giovanni; Höglund, Mattias; Lindstrand, Anders; Mertens, Fredrik

doi:10.1038/modpathol.3880308

Cited by 12 publications

(4 citation statements)

References 21 publications

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“…These proteins are believed to affect transcription as architectural elements by bending the DNA and by interacting with a large number of other proteins, mainly transcription factors, but also to influence chromatin changes during the cell cycle [27]. The HMGA2 gene is highly expressed in embryonic tissues but has in adults only been found expressed in kidney, lung, and synovia [7,11]. It has nevertheless been predicted to play a role in adult tissues as well [27].…”

Section: Discussionmentioning

confidence: 97%

Deregulation of HMGA2 in an aggressive angiomyxoma with t(11;12)(q23;q15)

et al. 2006

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Aggressive angiomyxoma is a soft-tissue neoplasm with a predilection for the pelvic and perineal regions and a tendency to recur locally. Cytogenetic data on this tumor type are limited to five cases, three of which showed rearrangement of chromosomal bands 12q13-15. Molecular investigation of two of the tumors identified the HMGA2 gene as the target of the 12q rearrangements. However, the two previously analyzed tumors were different at the molecular level: in one, the rearrangement of 12q13-15 resulted in a fusion product, whereas, in the second case, the breakpoint was telomeric (3') to the HMGA2, leaving the gene intact although expressed in its entire length. To shed more light on the pathobiology of aggressive angiomyxoma and to investigate the molecular mechanisms behind the involvement of the HMGA2 gene in this tumor type (fusion transcript vs deregulated expression), we investigated, cytogenetically and with molecular techniques, one such tumor which presented a t(11;12)(q23;q15) as the sole karyotypic aberration. FISH analyses demonstrated no structural alteration of HMGA2 at the cytogenetic level; however, expression of the full-length gene was detected molecularly.

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Section: Discussionmentioning

confidence: 97%

Deregulation of HMGA2 in an aggressive angiomyxoma with t(11;12)(q23;q15)

et al. 2006

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“…In conclusion, HMGA2 is known to play a major role in fetal growth and development, and its expression in adult tissues is restricted to lung, kidney, and synovia (Gattas, 1999;Broberg, 2001). A reactivation of the gene is involved in benign tumors of mesenchymal origin.…”

mentioning

confidence: 96%

Dysregulation and overexpression of HMGA2 in myelofibrosis with myeloid metaplasia

Andrieux

Demory

Dupriez

et al. 2003

Genes Chromosomes & Cancer

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Among cytogenetic studies of patients affected with myelofibrosis with myeloid metaplasia (MMM), a rare chronic myeloproliferative disorder, we found several reports of structural abnormalities of the long arm of chromosome 12. Two MMM patients had a balanced translocation involving 12q: t(4;12)(q32;q15) and t(5;12)(p14;q15), respectively. FISH (fluorescence in situ hybridization) analysis showed that BAC (bacterial artificial chromosome) RP11-366L20 overlaps the breakpoint in both cases. A gene, HMGA2, most of which is included in that BAC, thus was identified as a potential candidate. Using reserves transcriptase-polymerase chain reaction (RT-PCR), we looked for expression of HMGA2 in blood mononuclear cells from these 2 patients and demonstrated a transcript in both. Moreover, we found the gene expressed in the hematopoietic cells of 10 of 10 additional patients bearing no 12q anomalies. HMGA2, not expressed in normal subjects, is implicated in benign solid tumors such as lipomas, leiomyomas, and other rare tumors of mesenchymal origin. We postulate that its dysregulation and overexpression in myeloid progenitors contribute also to the pathogenesis of MMM.

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“…HMGA2 is highly expressed in the early developmental stage and participates in the differentiation of mesenchymal stem cells during fetal development ( 40 ). However, it remains silent in normal mature tissues, except for lung tissue, kidney tissue, and synovial tissue ( 41 , 42 ). The loss of epithelial markers and the acquisition of mesenchymal markers are typical characteristics of EMT, which play a key role in embryonic development ( 43 ).…”

Section: Physiological Function Of Hmga2mentioning

confidence: 99%

HMGA2 promotes cancer metastasis by regulating epithelial–mesenchymal transition

Ma,

Ye,

Liu

et al. 2024

Front. Oncol.

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Epithelial–mesenchymal transition (EMT) is a complex physiological process that transforms polarized epithelial cells into moving mesenchymal cells. Dysfunction of EMT promotes the invasion and metastasis of cancer. The architectural transcription factor high mobility group AT-hook 2 (HMGA2) is highly overexpressed in various types of cancer (e.g., colorectal cancer, liver cancer, breast cancer, uterine leiomyomas) and significantly correlated with poor survival rates. Evidence indicated that HMGA2 overexpression markedly decreased the expression of epithelial marker E-cadherin (CDH1) and increased that of vimentin (VIM), Snail, N-cadherin (CDH2), and zinc finger E-box binding homeobox 1 (ZEB1) by targeting the transforming growth factor beta/SMAD (TGFβ/SMAD), mitogen-activated protein kinase (MAPK), and WNT/beta-catenin (WNT/β-catenin) signaling pathways. Furthermore, a new class of non-coding RNAs (miRNAs, circular RNAs, and long non-coding RNAs) plays an essential role in the process of HMGA2-induced metastasis and invasion of cancer by accelerating the EMT process. In this review, we discuss alterations in the expression of HMGA2 in various types of cancer. Furthermore, we highlight the role of HMGA2-induced EMT in promoting tumor growth, migration, and invasion. More importantly, we discuss extensively the mechanism through which HMGA2 regulates the EMT process and invasion in most cancers, including signaling pathways and the interacting RNA signaling axis. Thus, the elucidation of molecular mechanisms that underlie the effects of HMGA2 on cancer invasion and patient survival by mediating EMT may offer new therapeutic methods for preventing cancer progression.

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The Tumor-Associated Gene HMGIC Is Expressed in Normal and Osteoarthritis-Affected Synovia

Cited by 12 publications

References 21 publications

Deregulation of HMGA2 in an aggressive angiomyxoma with t(11;12)(q23;q15)

Deregulation of HMGA2 in an aggressive angiomyxoma with t(11;12)(q23;q15)

Dysregulation and overexpression of HMGA2 in myelofibrosis with myeloid metaplasia

HMGA2 promotes cancer metastasis by regulating epithelial–mesenchymal transition

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