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Auriculasin-induced ROS causes prostate cancer cell death via induction of apoptosis
Hyun-Dong Cho1, Ju-Hye Lee2, Kwang-Deog Moon1
1Department of Food Science and Technology, Kyungpook National University, Daegu, 41566, Republic of Korea.
Abstract:
Recent studies have demonstrated that natural agents targeting the accumulation of reactive oxygen species (ROS) that selectively kill, leaving normal cells undamaged, can suppress prostate cancer. Here, we show that auriculasin, derived from Flemingia philippinensis, induces significant cell death and apoptosis via ROS generation in prostate cancer cells. Auriculasin treatment resulted in selective apoptotic cell death in LNCaP prostate cancer cells, characterized by DNA fragmentation, accumulation of sub-G1 cell population, cleavage of poly (ADP-ribose) polymerase (PARP), regulation of Bax/Bcl-2 ratio, increase of cytosolic apoptosis-inducing factor (AIF) and endonuclease G (EndoG), in addition to inhibiting tumor growth in a xenograft mouse model. Interestingly, auriculasin-induced apoptosis did not result in caspase-3, -8, and -9 activations. We found that auriculasin treatment decreased phosphorylation of AKT/mTOR/p70s6k in a dose- and time-dependent manner. Further, cellular ROS levels increased in LNCaP cells treated with auriculasin and blocking ROS accumulation with ROS scavengers resulted in inhibition of auriculasin-induced PARP cleavage, AIF increase, upregulation of Bax/Bcl-2 ratio, and decrease in AKT/mTOR phosphorylation. Taken together, these data suggest that auriculasin targets ROS-mediated caspase-independent pathways and suppresses PI3K/AKT/mTOR signaling, which leads to apoptosis and decreased tumor growth.
Insights
Auriculasin, a natural compound, effectively triggers cell death in prostate cancer by increasing reactive oxygen species (ROS). This compound selectively induces apoptosis and inhibits tumor growth without activating caspases.
Area of Science:
- Oncology
- Pharmacology
- Biochemistry
Background:
- Prostate cancer progression is linked to reactive oxygen species (ROS) accumulation.
- Natural agents offer potential for targeted cancer therapy by selectively eliminating cancer cells.
- Identifying novel compounds that induce cancer cell death is crucial for developing new treatments.
Purpose of the Study:
- To investigate the anti-cancer effects of auriculasin, a compound derived from Flemingia philippinensis.
- To elucidate the mechanism of action of auriculasin in prostate cancer cells, focusing on ROS generation and apoptosis induction.
- To evaluate the therapeutic potential of auriculasin in preclinical models of prostate cancer.
Main Methods:
- Treatment of LNCaP prostate cancer cells with auriculasin.
- Assessment of apoptosis markers including DNA fragmentation, sub-G1 population, PARP cleavage, Bax/Bcl-2 ratio, AIF, and EndoG.
- Analysis of caspase activation pathways (caspase-3, -8, -9).
- Evaluation of the PI3K/AKT/mTOR signaling pathway.
- Measurement of intracellular ROS levels and the effect of ROS scavengers.
- Inhibition of tumor growth in a xenograft mouse model.
Main Results:
- Auriculasin induced selective apoptotic cell death in LNCaP cells, evidenced by DNA fragmentation, PARP cleavage, and altered Bax/Bcl-2 ratio.
- Apoptosis occurred independently of caspase activation, involving increased AIF and EndoG.
- Auriculasin treatment suppressed PI3K/AKT/mTOR signaling pathway phosphorylation.
- Increased cellular ROS levels were observed, and ROS scavengers inhibited auriculasin-induced apoptosis and signaling pathway modulation.
- Auriculasin significantly inhibited tumor growth in a xenograft mouse model.
Conclusions:
- Auriculasin promotes prostate cancer cell apoptosis through ROS-mediated, caspase-independent pathways.
- The compound effectively suppresses tumor growth by modulating the PI3K/AKT/mTOR signaling pathway.
- Auriculasin demonstrates potential as a novel therapeutic agent for prostate cancer.
