The effect of IGF-I receptor blockade for human esophageal squamous cell carcinoma and adenocarcinoma View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

2013-09-13

AUTHORS

Yasushi Adachi, Hirokazu Ohashi, Arisa Imsumran, Hiroyuki Yamamoto, Yasutaka Matsunaga, Hiroaki Taniguchi, Katsuhiko Nosho, Hiromu Suzuki, Yasushi Sasaki, Yoshiaki Arimura, David P Carbone, Kohzoh Imai, Yasuhisa Shinomura

ABSTRACT

Insulin-like growth factor-I receptor (IGF-IR) signaling is required for carcinogenicity and tumor development, and this pathway has not been well studied in human esophageal carcinomas. Esophageal cancer is one of the human cancers with the worst prognosis and has two main histologies: squamous cell carcinomas (ESCC) and adenocarcinoma (EAC). Previously, we have reported that detection of the IGF axis may be useful for the prediction of recurrence and poor prognosis of ESCC. We have also shown the successful therapy for several gastrointestinal cancers using recombinant adenoviruses expressing dominant negative IGF-IR (ad-IGF-IR/dn). The aim of this study is to develop potential targeted therapeutics to IGF-IR and to assess the effect of IGF-IR blockade in both of these types of esophageal cancer. We determined immunohistochemical expression of IGF-IR in a tissue microarray. We then assessed the effect of IGF-IR blockade on signal transduction, proliferation, apoptosis, and motility. Ad-IGF-IR/dn, a tyrosine kinase inhibitor, BMS-536924, and adenovirus expressing shRNA for IGF-IR were used. IGF-IR expression was common in both tumor types but not in normal tissues. IGF-IR was detected in metastatic sites at similar levels compared to the primary site. IGF-IR inhibition suppressed proliferation and colony formation in both cancers. IGF-IR blockades up-regulated both stress- and chemotherapy-induced apoptosis and reduced migration. Although IGF-IR/dn blocked ligand-induced activation of Akt-1 mainly, BMS-536924 effectively blocked both activation of Akt and MAPK. The IGF axis might play a key role in tumor progression of esophageal carcinomas. The IGF-IR targeting strategies might thus be useful anticancer therapeutics for human esophageal malignancies. More... »

PAGES

973-985

Identifiers

URI

http://scigraph.springernature.com/pub.10.1007/s13277-013-1131-2

DOI

http://dx.doi.org/10.1007/s13277-013-1131-2

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1000207016

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/24026884


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27 schema:description Insulin-like growth factor-I receptor (IGF-IR) signaling is required for carcinogenicity and tumor development, and this pathway has not been well studied in human esophageal carcinomas. Esophageal cancer is one of the human cancers with the worst prognosis and has two main histologies: squamous cell carcinomas (ESCC) and adenocarcinoma (EAC). Previously, we have reported that detection of the IGF axis may be useful for the prediction of recurrence and poor prognosis of ESCC. We have also shown the successful therapy for several gastrointestinal cancers using recombinant adenoviruses expressing dominant negative IGF-IR (ad-IGF-IR/dn). The aim of this study is to develop potential targeted therapeutics to IGF-IR and to assess the effect of IGF-IR blockade in both of these types of esophageal cancer. We determined immunohistochemical expression of IGF-IR in a tissue microarray. We then assessed the effect of IGF-IR blockade on signal transduction, proliferation, apoptosis, and motility. Ad-IGF-IR/dn, a tyrosine kinase inhibitor, BMS-536924, and adenovirus expressing shRNA for IGF-IR were used. IGF-IR expression was common in both tumor types but not in normal tissues. IGF-IR was detected in metastatic sites at similar levels compared to the primary site. IGF-IR inhibition suppressed proliferation and colony formation in both cancers. IGF-IR blockades up-regulated both stress- and chemotherapy-induced apoptosis and reduced migration. Although IGF-IR/dn blocked ligand-induced activation of Akt-1 mainly, BMS-536924 effectively blocked both activation of Akt and MAPK. The IGF axis might play a key role in tumor progression of esophageal carcinomas. The IGF-IR targeting strategies might thus be useful anticancer therapeutics for human esophageal malignancies.
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34 Akt
35 Akt-1
36 BMS-536924
37 DN
38 ESCC
39 IGF axis
40 IGF-IR
41 IGF-IR blockade
42 IGF-IR expression
43 IGF-IR inhibition
44 IGF-IR/
45 MAPK
46 activation
47 activation of Akt
48 adenocarcinoma
49 adenovirus
50 aim
51 anticancer therapeutics
52 apoptosis
53 axis
54 blockade
55 cancer
56 carcinogenicity
57 carcinoma
58 cell carcinoma
59 chemotherapy-induced apoptosis
60 colony formation
61 detection
62 development
63 dominant negative IGF-IR
64 effect
65 esophageal cancer
66 esophageal carcinoma
67 esophageal malignancy
68 esophageal squamous cell carcinoma
69 expression
70 formation
71 gastrointestinal cancer
72 histology
73 human cancers
74 human esophageal carcinoma
75 human esophageal squamous cell carcinoma
76 immunohistochemical expression
77 inhibition
78 inhibitors
79 insulin-like growth factor-I receptor (IGF-IR) signaling
80 key role
81 kinase inhibitors
82 levels
83 ligand-induced activation
84 main histology
85 malignancy
86 metastatic sites
87 microarray
88 migration
89 motility
90 normal tissues
91 pathway
92 poor prognosis
93 prediction
94 prediction of recurrence
95 primary site
96 prognosis
97 progression
98 proliferation
99 receptor blockade
100 receptor signaling
101 recombinant adenovirus
102 recurrence
103 role
104 shRNA
105 signal transduction
106 signaling
107 similar levels
108 sites
109 squamous cell carcinoma
110 strategies
111 stress
112 study
113 successful therapy
114 therapeutics
115 therapy
116 tissue
117 tissue microarray
118 transduction
119 tumor development
120 tumor progression
121 tumor types
122 types
123 tyrosine kinase inhibitors
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