PMID- 30218457
OWN - NLM
STAT- MEDLINE
DCOM- 20200117
LR  - 20200117
IS  - 1097-4652 (Electronic)
IS  - 0021-9541 (Linking)
VI  - 234
IP  - 3
DP  - 2019 Mar
TI  - Sodium selenite induces apoptosis via ROS-mediated NF-kappaB signaling and activation 
      of the Bax-caspase-9-caspase-3 axis in 4T1 cells.
PG  - 2511-2522
LID - 10.1002/jcp.26783 [doi]
AB  - Sodium selenite (SSE), a source of inorganic selenium, has been widely used as a 
      clinical cancer treatment, but the precise molecular mechanisms of SSE remain to 
      be elucidated. Our in vitro experiments have confirmed that SSE treatment causes 
      a transient increase in intracellular reactive oxygen species (ROS) levels, 
      resulting in the inhibition of nuclear transcription factor-kappaB (NF-kappaB) signaling 
      and p65 and nuclear factor of kappa light polypeptide gene enhancer in B-cells 
      inhibitor, alpha phosphorylation levels in 4T1 cells. The inhibition of NF-kappaB 
      subsequently increased the expression of the apoptosis gene B-cell 
      lymphoma-2-associated X (Bax) and downregulated the transcription of 
      antiapoptosis genes, such as B-cell lymphoma-2, cellular inhibitor of apoptosis 
      1, and X-linked inhibitor of apoptosis. Additionally, the accumulation of ROS 
      caused mitochondrial dysfunction, leading to the activation of caspase-9 and -3, 
      thereby resulting in apoptosis. However, modulation of the ROS level by the 
      chemical inhibitor N-acetyl-cysteine reversed these events. Similarly, in vitro 
      murine syngeneic breast tumor models showed that SSE inhibits tumor growth by 
      promoting apoptosis. These results indicate that SSE induces apoptosis via 
      ROS-mediated inhibition of NF-kappaB signaling and activation of the 
      Bax-caspase-9-caspase-3 axis.
CI  - (c) 2018 Wiley Periodicals, Inc.
FAU - Zhang, Tao
AU  - Zhang T
AUID- ORCID: 0000-0003-0006-0428
AD  - Department of Clinical Veterinary Medicine, College of Veterinary Medicine, 
      Huazhong Agricultural University, Wuhan, China.
FAU - Zhao, Gan
AU  - Zhao G
AD  - Department of Clinical Veterinary Medicine, College of Veterinary Medicine, 
      Huazhong Agricultural University, Wuhan, China.
FAU - Zhu, Xinying
AU  - Zhu X
AD  - Department of Clinical Veterinary Medicine, College of Veterinary Medicine, 
      Huazhong Agricultural University, Wuhan, China.
FAU - Jiang, Kangfeng
AU  - Jiang K
AD  - Department of Clinical Veterinary Medicine, College of Veterinary Medicine, 
      Huazhong Agricultural University, Wuhan, China.
FAU - Wu, Haichong
AU  - Wu H
AD  - Department of Clinical Veterinary Medicine, College of Veterinary Medicine, 
      Huazhong Agricultural University, Wuhan, China.
FAU - Deng, Ganzhen
AU  - Deng G
AD  - Department of Clinical Veterinary Medicine, College of Veterinary Medicine, 
      Huazhong Agricultural University, Wuhan, China.
FAU - Qiu, Changwei
AU  - Qiu C
AUID- ORCID: 0000-0002-7389-9534
AD  - Department of Clinical Veterinary Medicine, College of Veterinary Medicine, 
      Huazhong Agricultural University, Wuhan, China.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20180914
PL  - United States
TA  - J Cell Physiol
JT  - Journal of cellular physiology
JID - 0050222
RN  - 0 (NF-kappa B)
RN  - 0 (RELA protein, human)
RN  - 0 (Reactive Oxygen Species)
RN  - 0 (Transcription Factor RelA)
RN  - 0 (bcl-2-Associated X Protein)
RN  - EC 3.4.22.- (Caspase 3)
RN  - EC 3.4.22.- (Caspase 9)
RN  - HIW548RQ3W (Sodium Selenite)
SB  - IM
MH  - Animals
MH  - Apoptosis/genetics
MH  - Breast Neoplasms/*drug therapy/genetics/pathology
MH  - Caspase 3/genetics
MH  - Caspase 9/genetics
MH  - Cell Line, Tumor
MH  - Cell Proliferation/*drug effects
MH  - Gene Expression Regulation, Neoplastic/drug effects
MH  - Humans
MH  - Mammary Neoplasms, Animal/*drug therapy/genetics/pathology
MH  - Membrane Potential, Mitochondrial/drug effects
MH  - Mice
MH  - NF-kappa B/genetics
MH  - Phosphorylation/drug effects
MH  - Reactive Oxygen Species/metabolism
MH  - Signal Transduction/drug effects
MH  - Sodium Selenite/*pharmacology
MH  - Transcription Factor RelA/genetics
MH  - bcl-2-Associated X Protein/genetics
OTO - NOTNLM
OT  - apoptosis
OT  - breast cancer
OT  - nuclear transcription factor-kappaB (NF-kappaB)
OT  - reactive oxygen species (ROS)
OT  - sodium selenite (SSE)
EDAT- 2018/09/16 06:00
MHDA- 2020/01/18 06:00
CRDT- 2018/09/16 06:00
PHST- 2018/01/29 00:00 [received]
PHST- 2018/04/27 00:00 [accepted]
PHST- 2018/09/16 06:00 [pubmed]
PHST- 2020/01/18 06:00 [medline]
PHST- 2018/09/16 06:00 [entrez]
AID - 10.1002/jcp.26783 [doi]
PST - ppublish
SO  - J Cell Physiol. 2019 Mar;234(3):2511-2522. doi: 10.1002/jcp.26783. Epub 2018 Sep 
      14.