PMID- 28651126
OWN - NLM
STAT- MEDLINE
DCOM- 20180327
LR  - 20180327
IS  - 1096-0023 (Electronic)
IS  - 1043-4666 (Linking)
VI  - 97
DP  - 2017 Sep
TI  - TNF-alpha exerts cytotoxic effects on multidrug resistant breast cancer MCF-7/MX 
      cells via a non-apoptotic death pathway.
PG  - 167-174
LID - S1043-4666(17)30187-4 [pii]
LID - 10.1016/j.cyto.2017.06.014 [doi]
AB  - Tumor necrosis factor-alpha (TNF-alpha) is a cytokine involved in the various 
      physiopathological processes such as autoimmune disorders and inflammation 
      related diseases. Some multidrug resistant (MDR) cancer cell lines including 
      MCF-7/MX are more vulnerable to cytotoxic effects of TNF-alpha than their parental 
      lines. In this study, breast cancer cell line MCF-7 and its MDR derivative 
      MCF-7/MX were exposed to TNF-alpha afterward various downstream signaling mediators 
      of TNF-alpha were analyzed. Although, treatment of MCF-7 cells with TNF-alpha activated 
      NF-kB and caused RIP1 ubiquitination, TNF-alpha exposure led to JNK and RIP1 
      phosphorylation in MCF-7/MX cells. In both cell lines TNF-alpha did not activate the 
      caspase cascade. Moreover, AnexinV/PI analysis showed that cytotoxic effects of 
      TNF-alpha on MCF-7/MX is mediated via apoptosis independent mechanisms and inhibition 
      of RIP1 kinase activity using necrostatin-1 revealed that kinase activity of RIP1 
      plays role in the production of ROS, activation of JNK and cellular death 
      following exposure of MCF-7/MX cells to TNF-alpha. Overall, it seems that RIP1 
      ubiquitination and NF-kB activation are prosurvival signaling mediators 
      protecting MCF-7 cells against cytotoxic effects of TNF-alpha while TNF-alpha drives 
      MCF-7/MX cells to non-apoptotic cellular death via kinase activity of RIP1, 
      activation of JNK and ROS production.
CI  - Copyright (c) 2017 Elsevier Ltd. All rights reserved.
FAU - Ghandadi, Morteza
AU  - Ghandadi M
AD  - Department of Pharmacognosy and Biotechnology, Faculty of Pharmacy, Mazandaran 
      University of Medical Sciences, Sari, Iran.
FAU - Behravan, Javad
AU  - Behravan J
AD  - Biotechnology Research Center, Mashhad University of Medical Sciences, Mashhad, 
      Iran; Department of Pharmaceutical Biotechnology, School of Pharmacy, Mashhad 
      University of Medical Sciences, Mashhad, Iran.
FAU - Abnous, Khalil
AU  - Abnous K
AD  - Pharmaceutical Research Center, Mashhad University of Medical Sciences, Mashhad, 
      Iran.
FAU - Ehtesham Gharaee, Melika
AU  - Ehtesham Gharaee M
AD  - Department of Pharmaceutical Biotechnology, School of Pharmacy, Mashhad 
      University of Medical Sciences, Mashhad, Iran.
FAU - Mosaffa, Fatemeh
AU  - Mosaffa F
AD  - Biotechnology Research Center, Mashhad University of Medical Sciences, Mashhad, 
      Iran; Department of Pharmaceutical Biotechnology, School of Pharmacy, Mashhad 
      University of Medical Sciences, Mashhad, Iran. Electronic address: 
      mosaffaf@mums.ac.ir.
LA  - eng
PT  - Journal Article
DEP - 20170623
PL  - England
TA  - Cytokine
JT  - Cytokine
JID - 9005353
RN  - 0 (AGFG1 protein, human)
RN  - 0 (NF-kappa B)
RN  - 0 (Nuclear Pore Complex Proteins)
RN  - 0 (Proto-Oncogene Proteins)
RN  - 0 (RNA-Binding Proteins)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - EC 2.7.10.1 (Protein-Tyrosine Kinases)
RN  - EC 2.7.10.1 (ROS1 protein, human)
RN  - EC 2.7.12.2 (MAP Kinase Kinase 4)
SB  - IM
MH  - Apoptosis
MH  - Cell Death/*drug effects
MH  - Cell Survival/*drug effects
MH  - *Drug Resistance, Neoplasm
MH  - Female
MH  - Humans
MH  - MAP Kinase Kinase 4/metabolism
MH  - MCF-7 Cells
MH  - NF-kappa B/metabolism
MH  - Nuclear Pore Complex Proteins/metabolism
MH  - Phosphorylation
MH  - Protein-Tyrosine Kinases/metabolism
MH  - Proto-Oncogene Proteins/metabolism
MH  - RNA-Binding Proteins/metabolism
MH  - Signal Transduction/*drug effects
MH  - Tumor Necrosis Factor-alpha/*pharmacology
OTO - NOTNLM
OT  - Breast cancer
OT  - Multidrug resistance
OT  - RIP1
OT  - ROS
OT  - TNF-alpha
EDAT- 2017/06/27 06:00
MHDA- 2018/03/28 06:00
CRDT- 2017/06/27 06:00
PHST- 2017/02/10 00:00 [received]
PHST- 2017/06/07 00:00 [revised]
PHST- 2017/06/20 00:00 [accepted]
PHST- 2017/06/27 06:00 [pubmed]
PHST- 2018/03/28 06:00 [medline]
PHST- 2017/06/27 06:00 [entrez]
AID - S1043-4666(17)30187-4 [pii]
AID - 10.1016/j.cyto.2017.06.014 [doi]
PST - ppublish
SO  - Cytokine. 2017 Sep;97:167-174. doi: 10.1016/j.cyto.2017.06.014. Epub 2017 Jun 23.