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In pleomorphic adenomas of the salivary glands (PASG) recurrent chromosomal rearrangements affecting either 8q12 or 12q14∼15 lead to an overexpression of the genes of the genuine transcription factor PLAG1 or the architectural transcription factor HMGA2, respectively. Both genes are also affected by recurrent chromosomal rearrangements in benign adipocytic tumors as e. g. lipomas and lipoblastomas. Herein, we observed a strong correlation between the expression of  HMGA2  and  PLAG1  in 14 benign and 23 malignant thyroid tumors. To address the question if  PLAG1  can be activated by HMGA2, the expression of both genes was quantified in 32 uterine leiomyomas 17 of which exhibited an overexpression of  HMGA2 . All leiomyomas with  HMGA2  overexpression also revealed an activation of  PLAG1  in the absence of detectable chromosome 8 abnormalities affecting the  PLAG1  locus. To further investigate if the overexpression of  PLAG1  is inducible by HMGA2 alone,  HMGA2  was transiently overexpressed in MCF-7 cells. An increased  PLAG1  expression was observed 24 and 48 h after transfection. Likewise, stimulation of  HMGA2  by FGF1 in adipose tissue-derived stem cells led to a simultaneous increase of  PLAG1  mRNA. Altogether, these data suggest that  HMGA2  is an upstream activator of  PLAG1 . Accordingly, this may explain the formation of tumors as similar as lipomas and lipoblastomas resulting from an activation of either of both genes by chromosomal rearrangements.

Correlated Expression of HMGA2 and PLAG1 in Thyroid Tumors, Uterine Leiomyomas and Experimental Models