PMID- 29387865
OWN - NLM
STAT- MEDLINE
DCOM- 20190104
LR  - 20190104
IS  - 1528-3658 (Electronic)
IS  - 1076-1551 (Print)
IS  - 1076-1551 (Linking)
VI  - 23
DP  - 2017 Nov
TI  - RAGE-aptamer Attenuates the Growth and Liver Metastasis of Malignant Melanoma in 
      Nude Mice.
PG  - 295-306
LID - 10.2119/molmed.2017.00099 [doi]
AB  - Epidemiological studies have suggested the link between cumulative diabetic 
      exposure and cancer. Interaction of advanced glycation end products (AGEs) with 
      their receptor (RAGE) may contribute to the phenomenon. We examined here the 
      effects of DNA aptamer raised against RAGE (RAGE-aptamer) on growth and liver 
      metastasis of G361 melanoma in nude mice. Malignant melanoma cells were 
      intradermally injected into the upper flank region of nude mice, which received 
      continuous administration of RAGE-aptamer (38.4 pmol/day/g body weight) or 
      vehicle intraperitoneally by an osmotic pump up to 42 days. RAGE-aptamer 
      significantly reduced levels of 8-hydroxy-2'-deoxy-guanosine, AGEs, RAGE, 
      proliferating nuclear antigen, cyclin D1, vascular endothelial growth factor 
      (VEGF), monocyte chemoattractant protein-1 (MCP-1), and CD31 and Mac-3, 
      respective markers of endothelial cells and macrophages in tumors of nude mice 
      and suppressed the proliferation and liver metastasis of malignant melanoma. 
      Furthermore, RAGE-aptamer attenuated the AGE-induced oxidative stress generation, 
      proliferation, and VEGF and MCP-1 gene expression in both G361 melanoma cells and 
      endothelial cells. The present findings suggest that RAGE-aptamer could attenuate 
      melanoma growth and liver metastasis in nude mice by suppressing the tumor 
      angiogenesis and macrophage infiltration via inhibition of the AGE-RAGE system. 
      RAGE-aptamer may be a novel therapeutic tool for the treatment of malignant 
      melanoma.
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 - Ishibashi, Yuji
AU  - Ishibashi 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 - Fukami, Kei
AU  - Fukami K
AD  - Department of Medicine, 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
AD  - Department of Pathophysiology and Therapeutics of Diabetic Vascular 
      Complications, Kurume University School of Medicine, Kurume, Japan.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20171106
PL  - England
TA  - Mol Med
JT  - Molecular medicine (Cambridge, Mass.)
JID - 9501023
RN  - 0 (Aptamers, Nucleotide)
RN  - 0 (Glycation End Products, Advanced)
RN  - 0 (Receptor for Advanced Glycation End Products)
SB  - IM
MH  - Animals
MH  - Aptamers, Nucleotide/*therapeutic use
MH  - Cell Line
MH  - Female
MH  - Glycation End Products, Advanced/metabolism
MH  - Humans
MH  - Liver Neoplasms/*prevention & control/secondary
MH  - Melanoma, Experimental/*drug therapy/metabolism/pathology
MH  - Mice, Nude
MH  - Neovascularization, Pathologic/*drug therapy
MH  - *Receptor for Advanced Glycation End Products
PMC - PMC5681699
OTO - NOTNLM
OT  - angiogenesis
OT  - carcinoma
OT  - diabetes
OT  - inflammation
OT  - liver
COIS- DISCLOSURE The authors declare that they have no competing interests as defined 
      by Molecular Medicine or other interests that might be perceived to influence the 
      results and discussion reported in this paper.
EDAT- 2018/02/02 06:00
MHDA- 2019/01/05 06:00
PMCR- 2017/11/06
CRDT- 2018/02/02 06:00
PHST- 2017/06/08 00:00 [received]
PHST- 2017/09/13 00:00 [accepted]
PHST- 2018/02/02 06:00 [pubmed]
PHST- 2019/01/05 06:00 [medline]
PHST- 2018/02/02 06:00 [entrez]
PHST- 2017/11/06 00:00 [pmc-release]
AID - molmed.2017.00099 [pii]
AID - 2017.00099 [pii]
AID - 10.2119/molmed.2017.00099 [doi]
PST - ppublish
SO  - Mol Med. 2017 Nov;23:295-306. doi: 10.2119/molmed.2017.00099. Epub 2017 Nov 6.