ECE2022 Poster Presentations Endocrine-Related Cancer (41 abstracts)
The transcriptomic and methylomic landscape of POU1F1 pituitary tumors
Gloria Elena Silva Román 1,2 , Ma Isabel Salazar 2 , Keiko Taniguchi Ponciano 1 , Juan Eduardo Peña Martínez 1 , Sandra Vela Patiño 1,2 , Sergio Andonegui Elguera 1 , Erick Gomez Apo 3 , Laura Chavez Macias 3,4 , Etual Espinosa Cardenas 1 , Claudia Ramirez Renteria 1 , Aldo Ferreira Hermosillo 1 , Ernesto Sosa 5 , Moises Mercado 1 & Daniel Marrero-Rodríguez 1
1Unidad de Investigación Medica en Enfermedades Endocrinas, Hospital de Especialidades, Centro Medico Nacional Siglo XXI, Instituto Mexicano del Seguro Social, Mexico City, Mexico; 2Departamento de Microbiología, Escuela Nacional de Ciencias Biológicas, Instituto Politécnico Nacional, Mexico City, Mexico; 3Área de Neuropatología, Servicio de Anatomía Patológica, Hospital General de México Dr. Eduardo Liceaga, Mexico City, Mexico; 4Facultad de Medicina, Universidad Nacional Autónoma de México, Mexico City, Mexico; 5Servicio de Endocrinología, Hospital de Especialidades, Centro Médico Nacional Siglo XXI, Instituto Mexicano del Seguro Social, Mexico City, Mexico
Pituitary adenomas (PA) are primarily benign lesions with monoclonal origins from the adenohypophyseal cells and represent 10-15% of all intracranial tumors. Tumors derived from POU1F1 cell lineage are GH-, TSH-, and PRL-secreting tumors that cause important syndromes such as acromegaly, hyperthyroidism, and sexual dysfunction, respectively. Surgical resection is the first line of treatment; the secondary treatment is pharmacological; despite having targets pharmacological in tumors derived of POU1F1 cell lineage, a high percentage of patient’s present resistance to pharmacotherapy over time. The molecular alterations continue unclearly understood. We performed global transcriptome and methylome profiling in six non-tumoral pituitary glands and sixteen POU1F1 tumors distributed as follows ten GH-, four TSH- and two PRL-tumors identifying differentially expressed genes regulated by methylation, miRNA-mRNA regulation, and pathway alterations. Our results showed distinctive transcriptome and methylome profiles segregating control glands from tumor samples. The transcriptomic analysis further revealed better segregation clusters according to the hormone-secreting tumor. We identified up-regulated coding genes such as DGKG, GRM5, and GPR173 common to the three tumors derived from the POU1F1 lineage. Interestingly, in each tumor identified up-regulated coding and non-coding genes such as CDKA5R1, MET, GRIN3A and miR4771-1 in PRL-; CHKA, TMEM233, miR95, LINC01347 and LINC01524 in GH-; NTRK3, GRIK4, miR4510, miR3925 and LINC00662 in TSH-secreting tumors, that could serve for future specific targets for molecular therapy. In addition, inside up-regulated genes we also identified hypomethylated status genes such as DGKG, miR590, miR4510, LINC00662, LINC01000, LINC01347, LINC01524; DNA hypomethylation in CPG islands in these genes potentially participates in up-regulated gene expression. miRNA-target gene found an interaction between miR590 with ANXA1, S100A10, YAP1, STAT3, ATP13A3, PTPN14, PCDG11X that also were identified down-regulated in our transcriptomic analysis. Pathway analysis revealed alterations in glycerophospholipids, phospholipase, and calcium signaling pathways. Overall, these results indicate potential molecular markers that could become specific targets for developing novel therapies.
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Endocrine Abstracts
ISSN 1470-3947 (print) | ISSN 1479-6848 (online)
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