Impaired Expression of Humanin during Adrenocortical Carcinoma

Author:

Blatkiewicz Małgorzata1ORCID,Szyszka Marta1ORCID,Olechnowicz Anna12ORCID,Kamiński Kacper12,Jopek Karol1ORCID,Komarowska Hanna3,Tyczewska Marianna14ORCID,Klimont Anna3,Wierzbicki Tomasz5,Karczewski Marek6,Ruchała Marek3ORCID,Rucinski Marcin1ORCID

Affiliation:

1. Department of Histology and Embryology, Poznan University of Medical Sciences, 60-781 Poznan, Poland

2. Doctoral School, Poznan University of Medical Sciences, 60-812 Poznan, Poland

3. Department of Endocrinology, Metabolism and Internal Medicine, Poznan University of Medical Sciences, 60-356 Poznan, Poland

4. Department of Anatomy and Histology, University of Zielona Góra, Licealna Street 9, 65-417 Zielona Góra, Poland

5. Department of General, Endocrinological and Gastroenterological Surgery, Poznan University of Medical Sciences, 60-355 Poznan, Poland

6. Department of General and Transplantation Surgery, Poznan University of Medical Sciences, 60-356 Poznan, Poland

Abstract

The discovery of mitochondria-derived peptides (MDPs) has provided a new perspective on mitochondrial function. MDPs encoded by mitochondrial DNA (mtDNA) can act as hormone-like peptides, influencing cell survival and proliferation. Among these peptides, humanin has been identified as a crucial factor for maintaining cell survival and preventing cell death under various conditions. Adrenocortical carcinoma (ACC) is a rare and aggressive malignancy that results from adrenal hormone dysfunction. This study aimed to investigate humanin expression in the adrenal tissue and serum of patients with ACC. For the first time, our study revealed significant reduction in the mRNA expression of humanin in patients with ACC compared to healthy controls. However, no significant changes were observed in the serum humanin levels. Interestingly, we identified a positive correlation between patient age and serum humanin levels and a negative correlation between tumor size and LDL levels. While the impaired expression of humanin in patients with ACC may be attributed to mitochondrial dysfunction, an alternative explanation could be related to diminished mitochondrial copy number. Further investigations are warranted to elucidate the intricate relationship among humanin, mitochondrial function, and ACC pathology.

Funder

National Science Centre

Publisher

MDPI AG

Subject

Inorganic Chemistry,Organic Chemistry,Physical and Theoretical Chemistry,Computer Science Applications,Spectroscopy,Molecular Biology,General Medicine,Catalysis

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