Abstract
Lambertianic acid (LA) is known to have anti-allergic and antibacterial effects. However, the anticancer activities and mechanism of action of LA have not been investigated. Therefore, the anticancer effects and mechanism of LA are investigated in this study. LA decreased not only AR protein levels, but also cellular and secretory levels of PSA. Furthermore, LA inhibited nuclear translocation of the AR induced by mibolerone. LA suppressed cell proliferation by inducing G1 arrest, downregulating CDK4/6 and cyclin D1 and activating p53 and its downstream molecules, p21 and p27. LA induced apoptosis and the expression of related proteins, including cleaved caspase-9 and -3, c-PARP and BAX, and inhibited BCl-2. The role of AR in LA-induced apoptosis was assessed by using siRNA. Collectively, these findings suggest that LA exerts the anticancer effect by inhibiting AR and is a valuable therapeutic agent in prostate cancer treatment.
Highlights
Prostate cancer is the second most common form of cancer in males and a direct cause of death in men worldwide [1,2]
Previous studies show that anti-spermatogenesis, anticancer activity and apoptosis in prostate cancer cells were induced by the suppression of androgen receptor (AR) signaling [11,12,13]
Lambertianic acid was originally isolated and identified from Pinus koraiensis Siebold and Zucc (Pinaceae) [17]; our previous studies showed that it exerts anti-obesity effects [18]
Summary
Prostate cancer is the second most common form of cancer in males and a direct cause of death in men worldwide [1,2]. The AR, the role of which was demonstrated in the late 1960s, conducts an important role in the growth and proliferation of androgen-dependent prostate cancer and cells [5,6,7]. AR regulates the prostate-specific antigen (PSA) expression in prostate cancer cells [8,9]. Previous studies show that anti-spermatogenesis, anticancer activity and apoptosis in prostate cancer cells were induced by the suppression of AR signaling [11,12,13]. Several studies have reported that p53 regulates the AR, transcription of PSA [14] and induces AR downregulation in prostate cancer [15]. The purpose of the present study was to investigate the anticancer activity of LA likely mediated via the AR pathway in LNCaP cells
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