PMID- 31565056
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20201001
IS  - 1687-8450 (Print)
IS  - 1687-8469 (Electronic)
IS  - 1687-8450 (Linking)
VI  - 2019
DP  - 2019
TI  - Long-Term Local Injection of RAGE-Aptamer Suppresses the Growth of Malignant 
      Melanoma in Nude Mice.
PG  - 7387601
LID - 10.1155/2019/7387601 [doi]
LID - 7387601
AB  - Accumulating evidence has suggested the pathological role of advanced glycation 
      end products (AGEs) and their receptor RAGE axis in aging-associated disorders, 
      including cancers. In this study, we examined the effects of local injection of 
      RAGE-aptamer adjacent to the tumor on G361 melanoma growth in nude mice. We 
      further investigated the effects of RAGE-aptamer on oxidative stress generation, 
      RAGE, vascular endothelial growth factor (VEGF), and monocyte chemoattractant 
      protein-1 (MCP-1) gene expression in N (epsilon) -(carboxymethyl)lysine (CML)-exposed 
      G361 melanoma cells in vitro. Local injection of RAGE-aptamer adjacent to the 
      tumor dramatically decreased the growth of G361 melanoma in nude mice, which was 
      associated with reduced expression of CML, RAGE, nitrotyrosine, VEGF, CD31, and 
      von Willebrand factor, markers of endothelial cells in G361 tumors. Furthermore, 
      RAGE-aptamer inhibited the binding of CML to V-domain of RAGE and blocked the 
      CML-induced increases in oxidative stress generation, RAGE, VEGF, and MCP-1 mRNA 
      levels in G361 melanoma cells. Our present findings suggest that long-term local 
      injection of RAGE-aptamer adjacent to the tumor could inhibit melanoma growth in 
      nude mice partly by suppressing tumor angiogenesis via blockade of the CML-RAGE 
      interaction. Local injection of RAGE-aptamer may be a feasible therapeutic tool 
      for the treatment of malignant melanoma.
CI  - Copyright (c) 2019 Nobutaka Nakamura et al.
FAU - Nakamura, Nobutaka
AU  - Nakamura N
AD  - Department of Pathophysiology and Therapeutics of Diabetic Vascular 
      Complications, Kurume University School of Medicine, Kurume, Japan.
FAU - Matsui, Takanori
AU  - Matsui T
AD  - Department of Pathophysiology and Therapeutics of Diabetic Vascular 
      Complications, Kurume University School of Medicine, Kurume, Japan.
FAU - Nishino, Yuri
AU  - Nishino Y
AD  - Department of Pathophysiology and Therapeutics of Diabetic Vascular 
      Complications, Kurume University School of Medicine, Kurume, Japan.
FAU - Sotokawauchi, Ami
AU  - Sotokawauchi A
AD  - Department of Pathophysiology and Therapeutics of Diabetic Vascular 
      Complications, Kurume University School of Medicine, Kurume, Japan.
FAU - Higashimoto, Yuichiro
AU  - Higashimoto Y
AD  - Department of Chemistry, Kurume University School of Medicine, Kurume, Japan.
FAU - Yamagishi, Sho-Ichi
AU  - Yamagishi SI
AUID- ORCID: 0000-0003-0102-0823
AD  - Division of Diabetes, Metabolism, and Endocrinology, Department of Medicine, 
      Showa University School of Medicine, Tokyo, Japan.
LA  - eng
PT  - Journal Article
DEP - 20190904
PL  - Egypt
TA  - J Oncol
JT  - Journal of oncology
JID - 101496537
PMC - PMC6746150
COIS- The authors declare that there are no conflicts of interest.
EDAT- 2019/10/01 06:00
MHDA- 2019/10/01 06:01
PMCR- 2019/09/04
CRDT- 2019/10/01 06:00
PHST- 2018/11/19 00:00 [received]
PHST- 2019/05/12 00:00 [revised]
PHST- 2019/08/08 00:00 [accepted]
PHST- 2019/10/01 06:00 [entrez]
PHST- 2019/10/01 06:00 [pubmed]
PHST- 2019/10/01 06:01 [medline]
PHST- 2019/09/04 00:00 [pmc-release]
AID - 10.1155/2019/7387601 [doi]
PST - epublish
SO  - J Oncol. 2019 Sep 4;2019:7387601. doi: 10.1155/2019/7387601. eCollection 2019.