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1.
Braz J Med Biol Res ; 52(4): e7728, 2019.
Artigo em Inglês | MEDLINE | ID: mdl-30994730

RESUMO

Pituitary adenoma is one of the most common tumors in the neuroendocrine system. This study investigated the effects of long non-coding RNAs (lncRNAs) highly up-regulated in liver cancer (HULC) on rat secreting pituitary adenoma GH3 cell viability, migration, invasion, apoptosis, and hormone secretion, as well as the underlying potential mechanisms. Cell transfection and qRT-PCR were used to change and measure the expression levels of HULC, miR-130b, and FOXM1. Cell viability, migration, invasion, and apoptosis were assessed using trypan blue staining assay, MTT assay, two-chamber transwell assay, Guava Nexin assay, and western blotting. The concentrations of prolactin (PRL) and growth hormone (GH) in culture supernatant of GH3 cells were assessed using ELISA. The targeting relationship between miR-130b and FOXM1 was verified using dual luciferase activity. Finally, the expression levels of key factors involved in PI3K/AKT/mTOR and JAK1/STAT3 pathways were evaluated using western blotting. We found that HULC was highly expressed in GH3 cells. Overexpression of HULC promoted GH3 cell viability, migration, invasion, PRL and GH secretion, as well as activated PI3K/AKT/mTOR and JAK1/STAT3 pathways. Knockdown of HULC had opposite effects and induced cell apoptosis. HULC negatively regulated the expression of miR-130b, and miR-130b participated in the effects of HULC on GH3 cells. FOXM1 was a target gene of miR-130b, which was involved in the regulation of GH3 cell viability, migration, invasion, and apoptosis, as well as PI3K/AKT/mTOR and JAK1/STAT3 pathways. In conclusion, HULC tumor-promoting roles in secreting pituitary adenoma might be via down-regulating miR-130b, up-regulating FOXM1, and activating PI3K/AKT/mTOR and JAK1/STAT3 pathways.


Assuntos
Adenoma/patologia , Neoplasias Hipofisárias/patologia , RNA Longo não Codificante/fisiologia , Adenoma/genética , Adenoma/metabolismo , Animais , Apoptose/fisiologia , Western Blotting , Linhagem Celular Tumoral , Ensaios de Migração Celular , Movimento Celular/fisiologia , Sobrevivência Celular/fisiologia , Ensaio de Imunoadsorção Enzimática , Proteína Forkhead Box M1/análise , Proteína Forkhead Box M1/metabolismo , Humanos , Janus Quinase 1/análise , Janus Quinase 1/metabolismo , Luciferases , MicroRNAs/análise , MicroRNAs/metabolismo , Fosfatidilinositol 3-Quinases/análise , Fosfatidilinositol 3-Quinases/metabolismo , Neoplasias Hipofisárias/genética , Neoplasias Hipofisárias/metabolismo , Proteínas Proto-Oncogênicas c-akt/análise , Proteínas Proto-Oncogênicas c-akt/metabolismo , RNA Longo não Codificante/análise , Ratos , Reação em Cadeia da Polimerase Via Transcriptase Reversa , Fator de Transcrição STAT3/análise , Fator de Transcrição STAT3/metabolismo , Serina-Treonina Quinases TOR/análise , Serina-Treonina Quinases TOR/metabolismo , Transfecção
2.
Rev. bras. pesqui. méd. biol ; Braz. j. med. biol. res;52(4): e7728, 2019. graf
Artigo em Inglês | LILACS | ID: biblio-1001506

RESUMO

Pituitary adenoma is one of the most common tumors in the neuroendocrine system. This study investigated the effects of long non-coding RNAs (lncRNAs) highly up-regulated in liver cancer (HULC) on rat secreting pituitary adenoma GH3 cell viability, migration, invasion, apoptosis, and hormone secretion, as well as the underlying potential mechanisms. Cell transfection and qRT-PCR were used to change and measure the expression levels of HULC, miR-130b, and FOXM1. Cell viability, migration, invasion, and apoptosis were assessed using trypan blue staining assay, MTT assay, two-chamber transwell assay, Guava Nexin assay, and western blotting. The concentrations of prolactin (PRL) and growth hormone (GH) in culture supernatant of GH3 cells were assessed using ELISA. The targeting relationship between miR-130b and FOXM1 was verified using dual luciferase activity. Finally, the expression levels of key factors involved in PI3K/AKT/mTOR and JAK1/STAT3 pathways were evaluated using western blotting. We found that HULC was highly expressed in GH3 cells. Overexpression of HULC promoted GH3 cell viability, migration, invasion, PRL and GH secretion, as well as activated PI3K/AKT/mTOR and JAK1/STAT3 pathways. Knockdown of HULC had opposite effects and induced cell apoptosis. HULC negatively regulated the expression of miR-130b, and miR-130b participated in the effects of HULC on GH3 cells. FOXM1 was a target gene of miR-130b, which was involved in the regulation of GH3 cell viability, migration, invasion, and apoptosis, as well as PI3K/AKT/mTOR and JAK1/STAT3 pathways. In conclusion, HULC tumor-promoting roles in secreting pituitary adenoma might be via down-regulating miR-130b, up-regulating FOXM1, and activating PI3K/AKT/mTOR and JAK1/STAT3 pathways.


Assuntos
Humanos , Animais , Ratos , Neoplasias Hipofisárias/patologia , Adenoma/patologia , RNA Longo não Codificante/fisiologia , Ensaio de Imunoadsorção Enzimática , Transfecção , Adenoma/genética , Adenoma/metabolismo , Movimento Celular/fisiologia , Sobrevivência Celular/fisiologia , Western Blotting , Apoptose/fisiologia , MicroRNAs/análise , Linhagem Celular Tumoral , Fator de Transcrição STAT3/análise , Janus Quinase 1/análise , Janus Quinase 1/metabolismo , Ensaios de Migração Celular , Proteína Forkhead Box M1/análise , Proteína Forkhead Box M1/metabolismo , Luciferases
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