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Your search keyword '"BTB-POZ Domain"' showing total 2 results
Start Over Descriptor "BTB-POZ Domain" Journal acta pharmacologica sinica
2 results on '"BTB-POZ Domain"'

1. DUBR suppresses migration and invasion of human lung adenocarcinoma cells via ZBTB11-mediated inhibition of oxidative phosphorylation

Author

Lele Zhang, Baohui Han, Fangfei Qian, Wei Nie, Shuhui Cao, Jingwen Li, Minjuan Hu, Midie Xu, Yue Wang, Xueyan Zhang, Fang Hu, Changhui Li, Qin Zhang, and Jun Lu

Subjects
0301 basic medicine, Lung Neoplasms, Cell, Adenocarcinoma of Lung, Oxidative Phosphorylation, Article, Metastasis, 03 medical and health sciences, Structure-Activity Relationship, 0302 clinical medicine, Downregulation and upregulation, Cell Movement, medicine, Humans, Pharmacology (medical), Pharmacology, A549 cell, Gene knockdown, Dose-Response Relationship, Drug, Molecular Structure, Chemistry, Cell migration, General Medicine, medicine.disease, DNA-Binding Proteins, 030104 developmental biology, medicine.anatomical_structure, Cell culture, 030220 oncology & carcinogenesis, BTB-POZ Domain, Cancer research, Adenocarcinoma, RNA, Long Noncoding, Transcription Factors
Abstract

Long noncoding RNAs (lncRNAs) are involved in a variety of cancers, but the role of LncRNA DUBR in lung adenocarcinoma (LUAD), the most prevalent form of lung cancer, remains unclear. In this study we investigated the expression of DUBR in LUAD to ascertain its association with the clinical pathology and prognosis of LUAD. Analysis of mRNA expression in The Cancer Genome Atlas (TCGA) LUAD database and in-house LUAD cohort (n = 94) showed that DUBR was significantly downregulated in LUAD, and was associated with poor prognosis. In LUAD cell lines (H1975, A549), overexpression of DUBR significantly suppressed the migration and invasion of the LUAD cells. We demonstrated that c-Myc could bind to the promoter of DUBR, and transcriptionally suppressed its expression. Knockdown of c-Myc almost completely blocked the invasion and migration of LUAD cells, whereas knockdown of DUBR partially rescued c-Myc-knockdown suppressed cell migration and invasion. Furthermore, DUBR overexpression significantly increased the expression of a downstream protein of DUBR, zinc finger, and BTB domain containing 11 (ZBTB11), in H1975 and A549 cells; knockdown of ZBTB11 partially rescued the DUBR-overexpression suppressed cell migration and invasion; knockdown of c-Myc significantly upregulated the expression of ZBTB11 in LUAD cells. Finally, we revealed that DUBR/ZBTB11 axis suppressed oxidative phosphorylation in LUAD cells. In short, we demonstrate that c-Myc/DUBR/ZBTB11 axis suppresses migration and invasion of LUAD by attenuating cell oxidative phosphorylation, which provides new insights into the regulatory mechanism of DUBR.

Published
2020

2. DUBR suppresses migration and invasion of human lung adenocarcinoma cells via ZBTB11-mediated inhibition of oxidative phosphorylation.

Author

Nie W, Hu MJ, Zhang Q, Lu J, Qian FF, Zhang LL, Hu F, Li CH, Cao SH, Li JW, Wang Y, Zhang XY, Xu MD, and Han BH

Subjects
Adenocarcinoma of Lung diagnosis, BTB-POZ Domain, Cell Movement, DNA-Binding Proteins metabolism, Dose-Response Relationship, Drug, Humans, Lung Neoplasms diagnosis, Molecular Structure, Oxidative Phosphorylation, RNA, Long Noncoding genetics, Structure-Activity Relationship, Transcription Factors metabolism, Adenocarcinoma of Lung metabolism, Lung Neoplasms metabolism, RNA, Long Noncoding metabolism
Abstract

Long noncoding RNAs (lncRNAs) are involved in a variety of cancers, but the role of LncRNA DUBR in lung adenocarcinoma (LUAD), the most prevalent form of lung cancer, remains unclear. In this study we investigated the expression of DUBR in LUAD to ascertain its association with the clinical pathology and prognosis of LUAD. Analysis of mRNA expression in The Cancer Genome Atlas (TCGA) LUAD database and in-house LUAD cohort (n = 94) showed that DUBR was significantly downregulated in LUAD, and was associated with poor prognosis. In LUAD cell lines (H1975, A549), overexpression of DUBR significantly suppressed the migration and invasion of the LUAD cells. We demonstrated that c-Myc could bind to the promoter of DUBR, and transcriptionally suppressed its expression. Knockdown of c-Myc almost completely blocked the invasion and migration of LUAD cells, whereas knockdown of DUBR partially rescued c-Myc-knockdown suppressed cell migration and invasion. Furthermore, DUBR overexpression significantly increased the expression of a downstream protein of DUBR, zinc finger, and BTB domain containing 11 (ZBTB11), in H1975 and A549 cells; knockdown of ZBTB11 partially rescued the DUBR-overexpression suppressed cell migration and invasion; knockdown of c-Myc significantly upregulated the expression of ZBTB11 in LUAD cells. Finally, we revealed that DUBR/ZBTB11 axis suppressed oxidative phosphorylation in LUAD cells. In short, we demonstrate that c-Myc/DUBR/ZBTB11 axis suppresses migration and invasion of LUAD by attenuating cell oxidative phosphorylation, which provides new insights into the regulatory mechanism of DUBR., (© 2021. The Author(s), under exclusive licence to CPS and SIMM.)

Published
2022
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