Identification of Germline FOXE1 and Somatic MAPK Pathway Gene Alterations in Patients with Malignant Struma Ovarii, Cleft Palate and Thyroid Cancer.
Carolina PiresAna SaramagoMargarida M MouraJing LiSara DonatoInês J MarquesHélio BeloAna C MachadoRafael CabreraThomas G P GrünewaldValeriano LeiteBranca M CavacoPublished in: International journal of molecular sciences (2024)
Germline variants in the FOXE1 transcription factor have been associated with thyroid ectopy, cleft palate (CP) and thyroid cancer (TC). Here, we aimed to clarify the role of FOXE1 in Portuguese families (F1 and F2) with members diagnosed with malignant struma ovarii (MSO), an ovarian teratoma with ectopic malignant thyroid tissue, papillary TC (PTC) and CP. Two rare germline heterozygous variants in the FOXE1 promoter were identified: F1) c.-522G>C, in the proband (MSO) and her mother (asymptomatic); F2) c.9C>T, in the proband (PTC), her sister and her mother (CP). Functional studies using rat normal thyroid (PCCL3) and human PTC (TPC-1) cells revealed that c.9C>T decreased FOXE1 promoter transcriptional activity in both cell models, while c.-522G>C led to opposing activities in the two models, when compared to the wild type. Immunohistochemistry and RT-qPCR analyses of patients' thyroid tumours revealed lower FOXE1 expression compared to adjacent normal and hyperplastic thyroid tissues. The patient with MSO also harboured a novel germline AXIN1 variant, presenting a loss of heterozygosity in its benign and malignant teratoma tissues and observable β-catenin cytoplasmic accumulation. The sequencing of the F1 (MSO) and F2 (PTC) probands' tumours unveiled somatic BRAF and HRAS variants, respectively. Germline FOXE1 and AXIN1 variants might have a role in thyroid ectopy and cleft palate, which, together with MAPK pathway activation, may contribute to tumours' malignant transformation.
Keyphrases
- copy number
- transcription factor
- gene expression
- dna repair
- single cell
- wild type
- dna methylation
- signaling pathway
- oxidative stress
- genome wide
- case report
- endothelial cells
- end stage renal disease
- poor prognosis
- newly diagnosed
- cell proliferation
- ejection fraction
- epithelial mesenchymal transition
- chronic kidney disease
- induced apoptosis
- early onset
- dna binding
- cell therapy
- long non coding rna
- genome wide analysis
- case control
- genome wide identification