Introduction: The ACTH receptor (ACTHR) is primarily expressed in the adrenal cortex. Previous studies focused on the regulatory function of ACTHR in glucocorticoid secretion, but research on adrenal tumours is rare. The aim of this study was to evaluate ACTHR expression in common adrenal adenomas and investigate its influence on adrenal tumorigenesis using adrenocortical H295R cells.
Materials and methods: Real-time polymerase chain reaction and western blot were used to detect the expression of ACTHR in 18 aldosterone-producing adenomas, 16 cortisol-producing adenomas, 9 non-functional adenomas, and 12 normal adrenal samples. Lentiviral vector pLVX-mCMV-ACTHR-ZsGreen was transfected into the H295R cells to increase ACTHR expression. WST-1 and cell count were applied to evaluate cell proliferation at different ACTHR levels. TUNEL staining was used to measure cell apoptosis.
Results: Compared with normal adrenal samples, the aldosterone-producing adenoma samples had higher ACTHR mRNA and protein levels. However, the mRNA and protein levels of ACTHR in non-functional adenomas and cortisol-producing adenomas were lower than those in the normal adrenal samples. Proliferative activity in the experimental cells was higher than that in the control cells in the first three days. The proliferative activity peaked in the second day. However, this trend was reversed in the fourth day and became more apparent with time. By contrast, TUNEL staining showed that ACTHR overexpression did not induce a significant difference between the two groups.
Conclusions: Differential ACTHR expression may be determined by different types of adrenocortical tumours. ACTHR is more likely to have induced the proliferation rather than the apoptosis of H295R cells.
Keywords: Adrenal tumour; H295R cells; adrenocorticotropic hormone receptor; proliferation.