Implication of β2-adrenergic receptor and miR-196a correlation in neurite outgrowth of LNCaP prostate cancer cells

Abstract

The β2-adrenergic receptor has been shown to be involved in neuroendocrine differentiation and to contribute to the development of aggressive prostate cancer. In this study we have investigated whether miR-196a plays a role in the regulation of the β2-adrenergic receptor in the LNCaP prostate cancer cell line. Our results show that the expression of miR-196a is elevated in LNCaP prostate cancer cells with reduced levels of β2-adrenergic receptor after stably transfection with three different shRNAs. Furthermore, treatment with β-blockers showed that this upregulation is strictly related to the low levels of β2-adrenergic receptor and not to the inhibition of the receptor signaling activity. Finally, we found that the reduced ability of LNCaP cells with low levels of β2-adrenergic receptor to initiate neuroendocrine differentiation under androgen depletion conditions is mediated by miR-196a. In conclusion, this study provides the rational for a role of miR-196a in the β2-adrenergic receptor mediated neuroendocrine differentiation of LNCaP prostate cancer cells.

Inhibition of β2-adrenergic receptor regulates necroptosis in prostate cancer cell

“…The autonomic nervous system has been observed to exert a considerable impact on the development and progression [ 20 ]of prostate cancer. Studies have demonstrated a significant increase in sympathetic nerve activity [ 21 , 22 ]n tissues linked to high-risk prostate cancer, with β2AR [ 6 , 7 , 23 , 24 ] playing a vital role in the sympathetic nervous system signaling pathway. The analysis of the results revealed that patients who used propranolol for a long period of time experienced prolonged periods of survival [ 8 , 9 , 25 , 26 ].…”

Exploring the Potential of Rosemary Derived Compounds (Rosmarinic and Carnosic Acids) as Cancer Therapeutics: Current Knowledge and Future Perspectives

“…Furthermore, Petiwala’s study revealed that CA exhibited suppressive effects in prostate cancer by promoting proteasomal degradation of the androgen receptor (AR) by inducing ER stress ( Petiwala et al ., 2016 ). The androgen receptor is a molecular target for prostate cancer treatment; however, these receptors can develop resistance by increasing AR levels or inducing AR mutations for survival after androgen therapy ( Guerriero et al ., 2021 ).…”