PMID- 28739680
OWN - NLM
STAT- MEDLINE
DCOM- 20170810
LR  - 20201116
IS  - 1791-7530 (Electronic)
IS  - 0250-7005 (Linking)
VI  - 37
IP  - 8
DP  - 2017 Aug
TI  - BDNF: An Oncogene or Tumor Suppressor?
PG  - 3983-3990
AB  - Neurotrophins are a family of growth factors that are vital to the proper 
      development of the central nervous system. Their effects on cells are governed by 
      the expression and activation of the tyrosine kinase receptors TrkA, TrkB and 
      TrkC. TrkB has been immensely implicated in mediating neuronal migration, 
      development and differentiation. It has also been shown to protect several 
      neuronal cell types from an array of cytotoxic stressors after activation by its 
      conjugate ligand brain-derived neurotrophic factor (BDNF). Over the past two 
      decades, it has been shown that TrkB and BDNF are up-regulated in many types of 
      cancers, conferring aggressive phenotypes underpinned by their resistance to 
      several standard chemotherapeutic agents. This resistance to chemotherapy is 
      modulated by the downstream targets of the TrkB receptor which include the 
      well-characterized PI3K /Akt growth pathway, a hallmark of uncontrolled cancer 
      cell growth and proliferation. Pre-clinical efforts to develop inhibitors of this 
      receptor are promising, and such inhibitors also seem to sensitize cancer cells 
      to standard chemotherapies. However, new evidence suggests that BDNF 
      overexpression in the hypothalamus has immunoaugmenting properties, eliciting an 
      increased anti-tumor immune response and reducing the activity of several 
      proteins that would normally confer resistance to chemotherapeutic agents. In the 
      current work, we provide a global analysis of the physiological consequences of 
      TrkB receptor activation in vitro and discuss the dynamic consequences of TrkB 
      activation in vivo. Finally, we propose a clinically-feasible option for 
      increasing BDNF expression in the hypothalamus to more readily utilize the 
      oncolytic effects of BDNF.
CI  - Copyright(c) 2017, International Institute of Anticancer Research (Dr. George J. 
      Delinasios), All rights reserved.
FAU - Radin, Daniel P
AU  - Radin DP
AD  - Department of Pharmacology, Stony Brook University School of Medicine, Stony 
      Brook, NY, U.S.A. danradin1@gmail.com.
FAU - Patel, Parth
AU  - Patel P
AD  - College of Arts and Sciences, New York University, New York City, NY, U.S.A.
LA  - eng
PT  - Journal Article
PT  - Review
PL  - Greece
TA  - Anticancer Res
JT  - Anticancer research
JID - 8102988
RN  - 0 (Brain-Derived Neurotrophic Factor)
RN  - 0 (Membrane Glycoproteins)
RN  - 0 (NTRK1 protein, human)
RN  - 7171WSG8A2 (BDNF protein, human)
RN  - EC 2.7.10.1 (Protein-Tyrosine Kinases)
RN  - EC 2.7.10.1 (Receptor, trkA)
RN  - EC 2.7.10.1 (Receptor, trkB)
RN  - EC 2.7.10.1 (Receptor, trkC)
RN  - EC 2.7.10.1 (tropomyosin-related kinase-B, human)
SB  - IM
MH  - Brain-Derived Neurotrophic Factor/biosynthesis/*genetics
MH  - Drug Resistance, Neoplasm/genetics
MH  - Gene Expression Regulation, Neoplastic
MH  - Genes, Tumor Suppressor
MH  - Humans
MH  - Hypothalamus/metabolism
MH  - Membrane Glycoproteins/biosynthesis/*genetics
MH  - Neoplasms/*drug therapy/*genetics/pathology
MH  - Oncogenes/genetics
MH  - Protein-Tyrosine Kinases/biosynthesis/*genetics
MH  - Receptor, trkA/biosynthesis/genetics
MH  - Receptor, trkB
MH  - Receptor, trkC/biosynthesis/genetics
OTO - NOTNLM
OT  - BDNF
OT  - EGFR
OT  - PI3K
OT  - RhoA
OT  - Trkb
OT  - chemotherapeutic resistance
OT  - review
EDAT- 2017/07/26 06:00
MHDA- 2017/08/11 06:00
CRDT- 2017/07/26 06:00
PHST- 2017/06/01 00:00 [received]
PHST- 2017/06/16 00:00 [revised]
PHST- 2017/06/19 00:00 [accepted]
PHST- 2017/07/26 06:00 [entrez]
PHST- 2017/07/26 06:00 [pubmed]
PHST- 2017/08/11 06:00 [medline]
AID - 37/8/3983 [pii]
AID - 10.21873/anticanres.11783 [doi]
PST - ppublish
SO  - Anticancer Res. 2017 Aug;37(8):3983-3990. doi: 10.21873/anticanres.11783.