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Salinomycin Induces Reactive Oxygen Species and Apoptosis in Aggressive Breast Cancer Cells as Mediated with Regulation of Autophagy.

Abstract Chemotherapy is a critical option for cancer treatment. However, consistent exposure to chemotherapeutic drugs promotes chemoresistance in cancer cells through diverse mechanisms. Accordingly, we investigated whether salinomycin, a monocarboxylic ionophore, could induce apoptosis in aggressive breast cancer cells or not, as well as its underlying mechanism.
PMID
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Authors

Mayor MeshTerms
Keywords

ROS

apoptosis

autophagy

breast cancer

chemoresistance

salinomycin

Journal Title anticancer research
Publication Year Start




PMID- 28373437
OWN - NLM
STAT- MEDLINE
DA  - 20170404
DCOM- 20170413
LR  - 20170413
IS  - 1791-7530 (Electronic)
IS  - 0250-7005 (Linking)
VI  - 37
IP  - 4
DP  - 2017 Apr
TI  - Salinomycin Induces Reactive Oxygen Species and Apoptosis in Aggressive Breast
      Cancer Cells as Mediated with Regulation of Autophagy.
PG  - 1747-1758
AB  - BACKGROUND/AIM: Chemotherapy is a critical option for cancer treatment. However, 
      consistent exposure to chemotherapeutic drugs promotes chemoresistance in cancer 
      cells through diverse mechanisms. Accordingly, we investigated whether
      salinomycin, a monocarboxylic ionophore, could induce apoptosis in aggressive
      breast cancer cells or not, as well as its underlying mechanism. MATERIALS AND
      METHODS: Using salinomycin on two breast cancer cell lines, MCF-7 cells and
      MDA-MB-231 cells, cell viability, annexin V/propidium iodide staining, acridine
      orange staining, caspase-3/9 activity, reactive oxygen species (ROS) and
      mitochondrial membrane potential (MMP) were assayed. RESULTS: In this study,
      salinomycin induced apoptosis and autophagy in MDA-MB-231 cells.
      Salinomycin-mediated ROS production led to mitochondrial dysfunction in
      MDA-MB-231 cells. Interestingly, treatment of N-acetyl-L-cysteine (NAC), a
      scavenger of ROS, attenuated salinomycin-induced apoptosis and autophagy.
      Moreover, autophagy inhibition is involved in acceleration of apoptosis induced
      by salinomycin. CONCLUSION: Salinomycin induced apoptosis and ROS production,
      that were blocked by autophagy, thus resulting in protecting cancer cells. This
      crosstalk of two different physiological responses (autophagy and apoptosis)
      induced by salinomycin might play pivotal roles in the relationship between
      autophagy and apoptosis of cancer cells.
CI  - Copyright(c) 2017, International Institute of Anticancer Research (Dr. George J. 
      Delinasios), All rights reserved.
FAU - Kim, Kwang-Youn
AU  - Kim KY
AD  - Department of Herbal Formula, Medical Research Center (MRC-GHF), College of
      Oriental Medicine, Daegu Haany University, Gyeongsan, Republic of Korea.
FAU - Park, Kwang Il
AU  - Park KI
AD  - Korean Medicine (KM)-Application Center, Korea Institute of Oriental Medicine
      (KIOM), Daegu, Republic of Korea.
FAU - Kim, Sang-Hun
AU  - Kim SH
AD  - Department of Microbiology and Immunology, Pusan National University School of
      Medicine, Yangsan, Republic of Korea.
FAU - Yu, Sun-Nyoung
AU  - Yu SN
AD  - Department of Microbiology and Immunology, Pusan National University School of
      Medicine, Yangsan, Republic of Korea.
FAU - Lee, Deokjae
AU  - Lee D
AD  - School of Life Sciences, Ulsan National Institute of Science and Technology,
      Ulsan, Republic of Korea.
FAU - Kim, Young Woo
AU  - Kim YW
AD  - Department of Herbal Formula, Medical Research Center (MRC-GHF), College of
      Oriental Medicine, Daegu Haany University, Gyeongsan, Republic of Korea.
FAU - Noh, Kyung Tae
AU  - Noh KT
AD  - Department of Infectious Diseases, Armed Forces Medical Research Institute,
      Daejeon, Republic of Korea.
FAU - Ma, Jin Yeul
AU  - Ma JY
AD  - Korean Medicine (KM)-Application Center, Korea Institute of Oriental Medicine
      (KIOM), Daegu, Republic of Korea.
FAU - Seo, Young-Kyo
AU  - Seo YK
AD  - School of Life Sciences, Ulsan National Institute of Science and Technology,
      Ulsan, Republic of Korea.
FAU - Ahn, Soon-Cheol
AU  - Ahn SC
AD  - Department of Microbiology and Immunology, Pusan National University School of
      Medicine, Yangsan, Republic of Korea [email protected]
LA  - eng
PT  - Journal Article
PL  - Greece
TA  - Anticancer Res
JT  - Anticancer research
JID - 8102988
RN  - 0 (Anti-Bacterial Agents)
RN  - 0 (Pyrans)
RN  - 0 (Reactive Oxygen Species)
RN  - 62UXS86T64 (salinomycin)
SB  - IM
MH  - Anti-Bacterial Agents/*pharmacology
MH  - Apoptosis/*drug effects
MH  - Autophagy/*drug effects
MH  - Blotting, Western
MH  - Breast Neoplasms/drug therapy/metabolism/*pathology
MH  - Cell Proliferation/drug effects
MH  - Female
MH  - Fluorescent Antibody Technique
MH  - Humans
MH  - Membrane Potential, Mitochondrial/drug effects
MH  - Pyrans/*pharmacology
MH  - Reactive Oxygen Species/*metabolism
MH  - Tumor Cells, Cultured
OTO - NOTNLM
OT  - *ROS
OT  - *apoptosis
OT  - *autophagy
OT  - *breast cancer
OT  - *chemoresistance
OT  - *salinomycin
EDAT- 2017/04/05 06:00
MHDA- 2017/04/14 06:00
CRDT- 2017/04/05 06:00
PHST- 2017/02/07 [received]
PHST- 2017/03/06 [revised]
PHST- 2017/03/07 [accepted]
AID - 37/4/1747 [pii]
AID - 10.21873/anticanres.11507 [doi]
PST - ppublish
SO  - Anticancer Res. 2017 Apr;37(4):1747-1758.

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