Biomolecules

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Special Issue Editors

Dr. Arulkumar Nagappan

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Guest Editor

Laboratory of Mucosal Exposome and Biomodulation, Department of Integrative Biomedical Sciences, Biomedical Research Institute, Pusan National University, Yangsan 50612, Korea
Interests: Bio-active compounds; Cancer metabolism; Apoptosis; Oxidative stress; Chemoresistance

Prof. Dr. Yuseok Moon

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Guest Editor

Laboratory of Mucosal Exposome and Biomodulation, Department of Integrative Biomedical Sciences, Biomedical Research Institute, Pusan National University, Yangsan 50612, Republic of Korea
Interests: immunotoxicity; mycotoxin; intestine; ribosome; mucosal immunology
Special Issues, Collections and Topics in MDPI journals

Dr. Ki Hyung Kim

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Guest Editor

Department of Obstetrics and Gynecology, Pusan National University School of Medicine, Busan, Korea
Interests: ovarian cancer; cervical cancer; ovarian; endometriosis; molecular mechanism

Special Issue Information

Dear Colleagues,

For the past two decades, bioactive compounds from plants, marine organisms, microorganisms, and endogenous factors have gained much attention in cancer treatment due to their significant efficacy and fewer adverse effects. In this context, recent research focused on the possibility of preventing or controlling cancer using bioactive compounds. Cancer is a leading cause of death in the world, accounting for about 10 million deaths in 2020. Chronic oxidative stress and inflammation have been implicated in the pathogenesis of several cancers. Cancer cells are known to manifest oxidative stress via abnormal energy metabolism including aerobic glycolysis (Warburg effect) or oxidative phosphorylation (OXPHOS) or both. Cancer metabolism-associated oxidative stress can account for cancer cells' survival and cell death; thus, the factors that regulate the homeostasis and/or dysregulation of oxidative signaling will be important biomarkers and therapeutic targets in cancer therapy. Therefore, bioactive compounds from natural herbs may alter the oxidative stress and the OXPHOS levels to interfere with the cancer formation, progression, or reoccurrence.

Dr. Arulkumar Nagappan
Prof. Dr. Yuseok Moon
Dr. Ki Hyung Kim
Guest Editors

Manuscript Submission Information

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Keywords

bioactive compounds
cancer
mitochondria
oxidative stress
cancer metabolism
apoptosis
metabolic reprogramming
OXPHOS
reactive oxygen species (ROS)
glycolysis
chemoresistance
therapeutics

Published Papers (2 papers)

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Research

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12 pages, 3904 KiB

Open AccessArticle

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, Un-Jung Yun, Seung-Hee Yeom, Sang-Chan Kim, Hu-Jang Lee, Soon-Cheol Ahn, Kwang-Il Park and Young-Woo Kim

Biomolecules 2021, 11(12), 1806; https://0-doi-org.brum.beds.ac.uk/10.3390/biom11121806 - 01 Dec 2021

Cited by 2 | Viewed by 1534

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. Full article

(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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Review

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15 pages, 1265 KiB

Open AccessReview

The Credible Role of Curcumin in Oxidative Stress-Mediated Mitochondrial Dysfunction in Mammals

by Muthuswamy Sathyabhama, Loganathan Chandramani Priya Dharshini, Adhimoolam Karthikeyan, Senthil Kalaiselvi and Taesun Min

Biomolecules 2022, 12(10), 1405; https://0-doi-org.brum.beds.ac.uk/10.3390/biom12101405 - 01 Oct 2022

Cited by 7 | Viewed by 2768

Abstract

Oxidative stress and mitochondrial dysfunction are associated with the pathogenesis of several human diseases. The excessive generation of reactive oxygen species (ROS) and/or lack of adequate antioxidant defenses causes DNA mutations in mitochondria, damages the mitochondrial respiratory chain, and alters membrane permeability and mitochondrial defense mechanisms. All these alterations are linked to the development of numerous diseases. Curcumin, an active ingredient of turmeric plant rhizomes, exhibits numerous biological activities (i.e., antioxidant, anti-inflammatory, anticancer, and antimicrobial). In recent years, many researchers have shown evidence that curcumin has the ability to reduce the oxidative stress- and mitochondrial dysfunction-associated diseases. In this review, we discuss curcumin’s antioxidant mechanism and significance in oxidative stress reduction and suppression of mitochondrial dysfunction in mammals. We also discuss the research gaps and give our opinion on how curcumin research in mammals should proceed moving forward. Full article

(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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