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Biomolecules
Volume 11
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10.3390/biom11121806
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Article

Inhibition of Autophagy Promotes Hemistepsin A-Induced Apoptosis via Reactive Oxygen Species-Mediated AMPK-Dependent Signaling in Human Prostate Cancer Cells

by
Kwang-Youn Kim
1,†,
Un-Jung Yun
2,†,
Seung-Hee Yeom
2,3,
Sang-Chan Kim
3,
Hu-Jang Lee
4,
Soon-Cheol Ahn
5,*,
Kwang-Il Park
4,* and
Young-Woo Kim
2,*
1
Korean Medicine (KM) Application Center, Korea Institute of Oriental Medicine, 70 Cheomdan-ro, Dong-gu, Daegu 41062, Korea
2
School of Korean Medicine, Dongguk University, Gyeongju 38066, Korea
3
Medical Research Center, College of Oriental Medicine, Daegu Haany University, Gyeongsan 38610, Korea
4
College of Veterinary Medicine, Gyeongsang National University, Jinju 52828, Korea
5
Department of Microbiology & Immunology, Pusan National University School of Medicine, Yangsan 50612, Korea
*
Authors to whom correspondence should be addressed.
†
Kwang-Youn Kim and Un-Jung Yun equally contributed to this work.
Biomolecules 2021, 11(12), 1806; https://doi.org/10.3390/biom11121806
Submission received: 22 October 2021 / Revised: 29 November 2021 / Accepted: 29 November 2021 / Published: 1 December 2021
(This article belongs to the Special Issue Role of Bioactive Compounds in the Regulation of Mitochondria and Oxidative Stress and Their Therapeutic Potential as Anti-cancer Agents)
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Abstract

Chemotherapy is an essential strategy for cancer treatment. On the other hand, consistent exposure to chemotherapeutic drugs induces chemo-resistance in cancer cells through a variety of mechanisms. Therefore, it is important to develop a new drug inhibiting chemo-resistance. Although hemistepsin A (HsA) is known to have anti-tumor effects, the molecular mechanisms of HsA-mediated cell death are unclear. Accordingly, this study examined whether HsA could induce apoptosis in aggressive prostate cancer cells, along with its underlying mechanism. Using HsA on two prostate cancer cell lines, PC-3 and LNCaP cells, the cell analysis and in vivo xenograft model were assayed. In this study, HsA induced apoptosis and autophagy in PC-3 cells. HsA-mediated ROS production attenuated HsA-induced apoptosis and autophagy after treatment with N-acetyl-L-cysteine (NAC), a ROS scavenger. Moreover, autophagy inhibition by 3-MA or CQ is involved in accelerating the apoptosis induced by HsA. Furthermore, we showed the anti-tumor effects of HsA in mice, as assessed by the reduced growth of the xenografted tumors. In conclusion, HsA induced apoptosis and ROS generation, which were blocked by protective autophagy signaling.
Keywords: Hemistepsin A; AMPK; ROS; autophagy; apoptosis; prostate cancer Hemistepsin A; AMPK; ROS; autophagy; apoptosis; prostate cancer

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MDPI and ACS Style

Kim, K.-Y.; Yun, U.-J.; Yeom, S.-H.; Kim, S.-C.; Lee, H.-J.; Ahn, S.-C.; Park, K.-I.; Kim, Y.-W. Inhibition of Autophagy Promotes Hemistepsin A-Induced Apoptosis via Reactive Oxygen Species-Mediated AMPK-Dependent Signaling in Human Prostate Cancer Cells. Biomolecules 2021, 11, 1806. https://doi.org/10.3390/biom11121806

AMA Style

Kim K-Y, Yun U-J, Yeom S-H, Kim S-C, Lee H-J, Ahn S-C, Park K-I, Kim Y-W. Inhibition of Autophagy Promotes Hemistepsin A-Induced Apoptosis via Reactive Oxygen Species-Mediated AMPK-Dependent Signaling in Human Prostate Cancer Cells. Biomolecules. 2021; 11(12):1806. https://doi.org/10.3390/biom11121806

Chicago/Turabian Style

Kim, Kwang-Youn, Un-Jung Yun, Seung-Hee Yeom, Sang-Chan Kim, Hu-Jang Lee, Soon-Cheol Ahn, Kwang-Il Park, and Young-Woo Kim. 2021. "Inhibition of Autophagy Promotes Hemistepsin A-Induced Apoptosis via Reactive Oxygen Species-Mediated AMPK-Dependent Signaling in Human Prostate Cancer Cells" Biomolecules 11, no. 12: 1806. https://doi.org/10.3390/biom11121806

APA Style

Kim, K.-Y., Yun, U.-J., Yeom, S.-H., Kim, S.-C., Lee, H.-J., Ahn, S.-C., Park, K.-I., & Kim, Y.-W. (2021). Inhibition of Autophagy Promotes Hemistepsin A-Induced Apoptosis via Reactive Oxygen Species-Mediated AMPK-Dependent Signaling in Human Prostate Cancer Cells. Biomolecules, 11(12), 1806. https://doi.org/10.3390/biom11121806

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