Activation of PLAG1 and HMGA2 by gene fusions involving the transcriptional regulator gene NFIB

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Afshari, Maryam K.Gothenburg University,Göteborgs universitet,Institutionen för biomedicin, avdelningen för laboratoriemedicin,Sahlgrenska Cancer Center,Department of Laboratory Medicine (author)

Activation of PLAG1 and HMGA2 by gene fusions involving the transcriptional regulator gene NFIB

Article/chapterEnglish2020

Publisher, publication year, extent ...

2020-08-05
Wiley,2020

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LIBRIS-ID:oai:gup.ub.gu.se/295462
https://gup.ub.gu.se/publication/295462URI
https://doi.org/10.1002/gcc.22885DOI

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Language:English

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SwePubSwePub

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Subject category:ref swepub-contenttype
Subject category:art swepub-publicationtype

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The pleomorphic adenoma (PA), which is the most common salivary gland neoplasm, is a benign tumor characterized by recurrent chromosome rearrangements involving 8q12 and 12q14-15. We have previously shown that thePLAG1andHMGA2oncogenes are the targets of these rearrangements. Here, we have identified previously unrecognized subsets of PAs with ins(9;8)/t(8;9) (n = 5) and ins(9;12)/t(9;12) (n = 8) and breakpoints located in the vicinity of thePLAG1andHMGA2loci. RNA-sequencing and reverse transcriptase (RT)-PCR analyses of a case with an ins(9;8) revealed a novelNFIB-PLAG1fusion in whichNFIBexon 4 is linked toPLAG1exon 3. In contrast to the developmentally regulatedPLAG1gene,NFIBwas highly expressed in normal salivary gland, indicating thatPLAG1in this case, as in other variant fusions, is activated by promoter swapping. RT-PCR analysis of three PAs with t(9;12) revealed two tumors with chimeric transcripts consisting ofHMGA2exon 4 linked toNFIBexons 9 or 3 and one case with a fusion linkingHMGA2exon 3 toNFIBexon 9. TheNFIBfusion events resulted in potent activation ofPLAG1andHMGA2. Analysis of the chromatin landscape surroundingNFIBrevealed several super-enhancers in the 5 '- and 3 '-parts of theNFIBlocus and its flanking sequences. These findings indicate thatPLAG1andHMGA2, similar toMYBin adenoid cystic carcinoma, may be activated by enhancer-hijacking events, in which super-enhancers inNFIBare translocated upstream ofPLAG1or downstream ofHMGA2. Our results further emphasize the role ofNFIBas a fusion partner to multiple oncogenes in histopathologically different types of salivary gland tumors.

Subject headings and genre

MEDICIN OCH HÄLSOVETENSKAP Medicinska och farmaceutiska grundvetenskaper Medicinsk genetik hsv//swe
MEDICAL AND HEALTH SCIENCES Basic Medicine Medical Genetics hsv//eng
MEDICIN OCH HÄLSOVETENSKAP Klinisk medicin Cancer och onkologi hsv//swe
MEDICAL AND HEALTH SCIENCES Clinical Medicine Cancer and Oncology hsv//eng
enhancer hijacking
gene fusion
HMGA2
NFIB
PLAG1
salivary
pleomorphic adenoma
adenoid cystic carcinoma
salivary-gland tumors
pleomorphic adenomas
chromosomal patterns
nfib
cell
histogenesis
specificity
expression
breast
Oncology
Genetics & Heredity

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Fehr, AndreGothenburg University,Göteborgs universitet,Institutionen för biomedicin, avdelningen för laboratoriemedicin,Sahlgrenska Cancer Center,Department of Laboratory Medicine(Swepub:gu)xfehra (author)
Nevado, PalomaGothenburg University,Göteborgs universitet,Sahlgrenska Cancer Center,Institutionen för biomedicin, avdelningen för laboratoriemedicin,Department of Laboratory Medicine(Swepub:gu)xtejpa (author)
Andersson, Mattias K,1979Gothenburg University,Göteborgs universitet,Institutionen för biomedicin, avdelningen för laboratoriemedicin,Sahlgrenska Cancer Center,Department of Laboratory Medicine(Swepub:gu)xamatx (author)
Stenman, Göran,1953Gothenburg University,Göteborgs universitet,Institutionen för biomedicin, avdelningen för laboratoriemedicin,Sahlgrenska Cancer Center,Department of Laboratory Medicine(Swepub:gu)xsteng (author)
Göteborgs universitetInstitutionen för biomedicin, avdelningen för laboratoriemedicin (creator_code:org_t)

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In:Genes Chromosomes & Cancer: Wiley59:11, s. 652-6601045-22571098-2264

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