Combined expression of BUB1B, DLGAP5, and PINK1 as predictors of poor outcome in adrenocortical tumors: validation in a Brazilian cohort of adult and pediatric patients

Fragoso, Maria Candida Barisson Villares; Almeida, Madson Q.; Mazzuco, Tânia Longo; Mariani, Beatriz M. P.; Brito, Luciana Pinto; Gonçalves, Talita Cardoso; Alencar, Guilherme Asmar; Lima, Lorena de Oliveira; Faria, André M.; Bourdeau, Isabelle; Lucon, Antônio Marmo; Freire, Daniel Soares; Latrônico, Ana Claudia; Mendonca, Berenice B.; Lacroix, André; Lerário, Antônio Marcondes

doi:10.1530/eje-11-0806

Cited by 80 publications

(70 citation statements)

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“…Similarly, the expression levels of DLG7 and PINK1 identified subgroups of ACCs with distinct disease-free survival, regardless of tumor grade (191). These findings were later validated in a separate cohort of adult patients (193).…”

Section: Gene Expression Arraysmentioning

confidence: 69%

Adrenocortical Carcinoma

et al. 2013

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Adrenocortical carcinoma (ACC) is a rare endocrine malignancy, often with an unfavorable prognosis. Here we summarize the knowledge about diagnosis, epidemiology, pathophysiology, and therapy of ACC. Over recent years, multidisciplinary clinics have formed and the first international treatment trials have been conducted. This review focuses on evidence gained from recent basic science and clinical research and provides perspectives from the experience of a large multidisciplinary clinic dedicated to the care of patients with ACC.

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Section: Gene Expression Arraysmentioning

confidence: 69%

Adrenocortical Carcinoma

et al. 2013

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“…CDK1 is regulated by CKIs (cyclin-dependent kinase inhibitors) such as p57 Kip2 , which is often downregulated coordinately with H19 in ACC (Gicquel et al, 1997; Heaton et al, 2012). BUB1B is overexpressed in ACC and the difference in the expression of BUB1B and PINK1 (PTEN-induced putative kinase 1) was strong predictor of overall survival in a group of adult ACCs (de Reynies et al, 2009; Fragoso et al, 2012). …”

Section: Resultsmentioning

confidence: 99%

POD-1 binding to the E-box sequence inhibits SF-1 and StAR expression in human adrenocortical tumor cells

França

Ferraz-de-Souza

Santos

et al. 2013

Molecular and Cellular Endocrinology

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Pod-1/Tcf21 is expressed at epithelial-mesenchymal interaction sites during development of many organs. Different approaches have demonstrated that Pod-1 transcriptionally inhibits Sf-1/NR5A1 during gonadal development. Disruption of Sf-1 can lead to disorders of adrenal development, while increased dosage of SF-1 has been related to increased adrenal cell proliferation and tumorigenesis. In this study, we analyzed whether POD-1 overexpression inhibits the endogenous Sf-1 expression in human and mouse adrenocortical tumor cells. Cells were transiently transfected with luciferase reporter gene under the control of Sf-1 promoter and with an expression vector encoding Pod-1. Pod-1 construct inhibited the transcription of the Sf1/Luc reporter gene in a dose-dependent manner in mouse Y-1 adrenocortical carcinoma (ACC) cells, and inhibited endogenous SF-1 expression in the human H295R and ACC-T36 adrenocortical carcinoma cells. These results were validated by chromatin immunoprecipitation assay with POD-1-transfected H295R cells using primers specific to E-box sequence in SF-1 promoter region, indicating that POD-1 binds to the SF-1 E-box promoter. Moreover, POD-1 over-expression resulted in a decrease in expression of the SF-1 target gene, StAR (Steroidogenic Acute Regulatory Protein). Lastly, while the induced expression of POD-1 did not affect the cell viability of H295R/POD-1 or ACC-T36/POD-1 cells, the most significantly enriched KEGG pathways for genes negatively correlated to POD-1/TCF21 in 33 human ACCs were those associated with cell cycle genes.

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“…These results further support the notion that Parkin may act as a tumor suppressor. The expression of another important mitophagy regulator, PINK1, has been reported to be linked to the survival and prognosis of the adrenocortical tumor (ACT) (52, 53). It was confirmed in a mouse model that knockdown of BNIP3 and NIX promotes tumor formation and metastasis (54, 55).…”

Section: Role Of Mitophagy In Human Diseasesmentioning

confidence: 99%

Emerging role of mitophagy in human diseases and physiology

Yun

2017

BMB Rep.

143

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Mitophagy is a process of selective removal of damaged or unnecessary mitochondria using autophagic machinery. Mitophagy plays an essential role in maintaining mitochondrial quality control and homeostasis. Mitochondrial dysfunctions and defective mitophagy in neurodegenerative diseases, cancer, and metabolic diseases indicate a close link between human disease and mitophagy. Furthermore, recent studies showing the involvement of mitophagy in differentiation and development, suggest that mitophagy may play a more active role in controlling cellular functions. A better understanding of mitophagy will provide insights about human disease and offer novel chance for treatment. This review mainly focuses on the recent implications for mitophagy in human diseases and normal physiology.

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Combined expression of BUB1B, DLGAP5, and PINK1 as predictors of poor outcome in adrenocortical tumors: validation in a Brazilian cohort of adult and pediatric patients

Cited by 80 publications

References 20 publications

Adrenocortical Carcinoma

Adrenocortical Carcinoma

POD-1 binding to the E-box sequence inhibits SF-1 and StAR expression in human adrenocortical tumor cells

Emerging role of mitophagy in human diseases and physiology

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