Abstract
Prostate cancer is the most common illness affecting men worldwide. Although much progress has been made in the study of prostate cancer prevention and treatment, less attention has been paid to the molecular mechanism of the disease. The molecular arrangement by which atractylenolide II (ATR II) induces human prostate cancer cytotoxicity was comprehensively examined in the present study. As indicated by the results, ATR II could inhibit prostate cancer cell proliferation and promote DU145 and LNCaP cell apoptosis through induced G2/M cell cycle arrest. The cell apoptosis process induced by ATR II in both DU145 and LNCaP cells was associated with its ability to inhibit androgen receptor (AR) with overexpression of protein inhibitor of activated STAT-1 (PIAS1) and the repression of Janus kinase (Jak2) signaling pathways. The data from the present study demonstrated the antitumor effects and the potential pharmacological application of ATR II as an efficient drug for prostate cancer treatment.
Highlights
Prostate cancer is the most common form of cancer diagnosed for men
Activation of androgen receptor (AR)-mediated by IL-6 does phosphoinositide 3-kane (PI3K) pathway is considered the main contributor to IL-6 signaling, its role not depend on the PI3K pathway [11]
G0/G1 and S percentages decreased decreased respectively for the same concentrations (Figure 2A). These results indicate that ATR IIinduced LNCaP and DU145 cells cycle arrest in the G2/M phase
Summary
Prostate cancer is the most common form of cancer diagnosed for men. This burden is related to some factors such as genomic, race, age as well as geographic localization [1]. The current treatments for prostate cancer include prostatectomy, chemotherapy, radiotherapy, and immunotherapy [2,3]. Plentiful clinical studies reported that in the early stage of prostate cancer, androgen signaling plays a pivotal role in the cells. A recent study [8] reported that a hormone depletion might regulate genes such as Akt and ERK1/2 activity in cancer cells to mediate androgen receptor AR down-regulation. It was reported that AR transactivation can be activated through IL-6 in human prostate cancer (LNCaP) cells in an androgen-independent manner [10]. Activation of AR-mediated by IL-6 does phosphoinositide 3-kane (PI3K) pathway is considered the main contributor to IL-6 signaling, its role not depend on the PI3K pathway [11]. Previous studiesand have been cancer through STAT3, nuclear factor kappa-light-chain-enhancer of cycle activated cells (NF-κB) gastric, signaling demonstrated that ATR. Provide a novel data for the application of ATR II in prostate cancer
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