This is a preprint, a preliminary version of a manuscript that has not completed peer review at a journal. Research Square does not conduct peer review prior to posting preprints. The posting of a preprint on this server should not be interpreted as an endorsement of its validity or suitability for dissemination as established information or for guiding clinical practice.
Research article
Anli Tong
Peking Union Medical College Hospital
Corresponding Author
License:
This work is licensed under a CC BY 4.0 License. Read Full License
Background: The evidence about effects of metformin on adrenocortical carcinoma cell lines is lacking. This study aims to investigate the effects of metformin on proliferation and secretion function of H295R cells.
Methods: H295R cells were treated with different doses of metformin for 3 days or with 20 mmol/L metformin for different times. Cell proliferation was detected by MTS method. Cortisol and aldosterone in culture medium was determined by chemiluminescent method and radioimmunoassay, respectively. H295R cells were treated with 20 mmol/L metformin for 24 hours, and mRNA expressions of 11 beta-hydroxylase (CYP11B1) and aldosterone synthase (CYP11B2) were detected by real-time quantitative PCR.
Results: The results showed that no differences of cell proliferation and secretion of cortisol and aldosterone were detected between control group and metformin group with doses less than 5 mmol/L. Metformin with large doses (≥ 10 mmol/L) significantly inhibited cell proliferation and secretion of cortisol and aldosterone in a dose-dependent pattern. Metformin (20 mmol/L) inhibited cell proliferation after 12 hours’ incubation. And the proliferation inhibitory effects of metformin were in a time-dependent manner. Compared with control group, metformin decreased secretion of cortisol and aldosterone, and mRNA expression of CYP11B1.
Conclusions: Metformin can inhibit cell proliferation and secretion of cortisol and aldosterone in H295R cells.
Keywords
metformin, H295R cell, cell proliferation, cortisol, aldosterone
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This is a preprint, a preliminary version of a manuscript that has not completed peer review at a journal. Research Square does not conduct peer review prior to posting preprints. The posting of a preprint on this server should not be interpreted as an endorsement of its validity or suitability for dissemination as established information or for guiding clinical practice.
Research article
Anli Tong
Peking Union Medical College Hospital
Corresponding Author
Badges
Prescreen
This manuscript passed our Prescreen assessment
Complete author information
Appropriate declaration statements
Potential risks to human health
Prescreen
History
CURRENT STATUS: Posted
Version 1
Posted 18 May, 2020
No community comments so far
Metrics
Comments: 0
PDF Downloads: ...
HTML Views: ...
Subject Areas
Endocrinology & Metabolism
License:
This work is licensed under a CC BY 4.0 License. Read Full License
Background: The evidence about effects of metformin on adrenocortical carcinoma cell lines is lacking. This study aims to investigate the effects of metformin on proliferation and secretion function of H295R cells.
Methods: H295R cells were treated with different doses of metformin for 3 days or with 20 mmol/L metformin for different times. Cell proliferation was detected by MTS method. Cortisol and aldosterone in culture medium was determined by chemiluminescent method and radioimmunoassay, respectively. H295R cells were treated with 20 mmol/L metformin for 24 hours, and mRNA expressions of 11 beta-hydroxylase (CYP11B1) and aldosterone synthase (CYP11B2) were detected by real-time quantitative PCR.
Results: The results showed that no differences of cell proliferation and secretion of cortisol and aldosterone were detected between control group and metformin group with doses less than 5 mmol/L. Metformin with large doses (≥ 10 mmol/L) significantly inhibited cell proliferation and secretion of cortisol and aldosterone in a dose-dependent pattern. Metformin (20 mmol/L) inhibited cell proliferation after 12 hours’ incubation. And the proliferation inhibitory effects of metformin were in a time-dependent manner. Compared with control group, metformin decreased secretion of cortisol and aldosterone, and mRNA expression of CYP11B1.
Conclusions: Metformin can inhibit cell proliferation and secretion of cortisol and aldosterone in H295R cells.
Figure 1
Figure 2
Figure 3
Figure 4
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