TY - JOUR
T1 - MicroRNA-149-3p expression correlates with outcomes of adrenocortical tumor patients and affects proliferation and cell cycle progression of H295A adrenocortical cancer cell line
AU - da Silva, Keteryne Rodrigues
AU - Veronez, Luciana Chain
AU - Correa, Carolina Alves Pereira
AU - Lira, Régia Caroline Peixoto
AU - Baroni, Mirella
AU - de Paula Silva Queiroz, Rosane
AU - Antonini, Sonir Roberto Rauber
AU - Yunes, José Andres
AU - Brandalise, Silvia Regina
AU - Tone, Luiz Gonzaga
AU - Scrideli, Carlos Alberto
N1 - Publisher Copyright:
© 2022, The Author(s) under exclusive licence to Japan Human Cell Society.
PY - 2022/11
Y1 - 2022/11
N2 - Pediatric adrenocortical tumor (ACT) is a rare and aggressive neoplasm, with incidence in southern and southeastern Brazil 10–15 times higher than worldwide. Although microRNAs (miRNAs) have been reported to act as tumor suppressors or oncogenes in several cancers, the role of miR-149-3p in ACT remains unknown. In this study, we evaluated the expression of miR-149-3p in 67 pediatric ACT samples and 19 non-neoplastic adrenal tissues. The overexpression of miR-149-3p was induced in H295A cell line, and cell viability, proliferation, colony formation, and cell cycle were assessed by in miR-149-3p mimic or mimic control. In silico analysis were used to predict miR-149-3p putative target genes. CDKN1A expression at the mRNA and protein levels was evaluated by qRT-PCR and western blot, respectively. Higher miR-149-3p expression was associated with unfavorable ACT outcomes. Compared to the mimic control, miR-149-3p overexpression increased cell viability and colony formation, and affected cell cycle progression. Also, we identified CDKN1A as a potential miR-149-3p target gene, with decreased expression at both the gene and protein levels in miR-149-3p mimic cells.
AB - Pediatric adrenocortical tumor (ACT) is a rare and aggressive neoplasm, with incidence in southern and southeastern Brazil 10–15 times higher than worldwide. Although microRNAs (miRNAs) have been reported to act as tumor suppressors or oncogenes in several cancers, the role of miR-149-3p in ACT remains unknown. In this study, we evaluated the expression of miR-149-3p in 67 pediatric ACT samples and 19 non-neoplastic adrenal tissues. The overexpression of miR-149-3p was induced in H295A cell line, and cell viability, proliferation, colony formation, and cell cycle were assessed by in miR-149-3p mimic or mimic control. In silico analysis were used to predict miR-149-3p putative target genes. CDKN1A expression at the mRNA and protein levels was evaluated by qRT-PCR and western blot, respectively. Higher miR-149-3p expression was associated with unfavorable ACT outcomes. Compared to the mimic control, miR-149-3p overexpression increased cell viability and colony formation, and affected cell cycle progression. Also, we identified CDKN1A as a potential miR-149-3p target gene, with decreased expression at both the gene and protein levels in miR-149-3p mimic cells.
KW - Adrenocortical tumors
KW - CDKN1A
KW - Cell cycle
KW - Cell viability
KW - microRNA
KW - miR-149-3p
UR - http://www.scopus.com/inward/record.url?scp=85137526230&partnerID=8YFLogxK
U2 - 10.1007/s13577-022-00778-2
DO - 10.1007/s13577-022-00778-2
M3 - Article
C2 - 36053456
AN - SCOPUS:85137526230
SN - 0914-7470
VL - 35
SP - 1952
EP - 1960
JO - Human Cell
JF - Human Cell
IS - 6
ER -