PMID- 23337790
OWN - NLM
STAT- MEDLINE
DCOM- 20130625
LR  - 20130122
IS  - 1881-7823 (Electronic)
IS  - 1881-7815 (Linking)
VI  - 6
IP  - 6
DP  - 2012 Dec
TI  - Effects of two monoclonal antibodies, MLS128 against Tn-antigen and 1H7 against 
      insulin-like growth factor-I receptor, on the growth of colon cancer cells.
PG  - 303-12
AB  - MLS128 is an anti-carbohydrate monoclonal antibody (mAb) that binds three or two 
      consecutive Tn-antigens. MLS128 bound 110-210 kDa glycoproteins (GPs) and 
      inhibited the growth of LS180 and HT29 colon and MCF-7 breast cancer cells. One 
      possible mechanism of MLS128's inhibition of growth may be via insulin-like 
      growth factor-I receptor (IGF-IR) down-regulation (Morita et al. BioScience 
      Trends. 2009; 3:32-37). The current study examined the role of IGF-IR signaling 
      in the growth of colon cancer cells and its possible interaction with 
      MLS128-induced inhibition of cell growth in LS180, LS174T, and HT29 human colon 
      cancer cells treated with MLS128 or anti-IGF-IR 1H7. Both MLS128 and 1H7 
      treatment significantly inhibited the growth of colon cancer cells. All three 
      colon cancer cell lines expressed IGF-IR. Their growth was in part IGF-I 
      dependent, but inhibition by MLS128 was independent of IGF-IR signaling. All of 
      the colon cancer cell lines expressed an 110kDa GP for MLS128 binding, but MCF-7 
      cells expressed MLS128-detectable bands with higher molecular masses. 1H7 
      treatments caused down-regulation of IGF-IR but did not affect 110kDa GP levels. 
      MLS128 treatments resulted in partial disappearance of the 110kDa band but did 
      not affect IGF-IR levels. Western blotting analyses of colon and breast cancer 
      cell lysates revealed that colon and breast cancer cells differed significantly 
      in patterns of expression of growth-related molecules while colon cancer cells 
      were similar but distinctive. In conclusion, MLS128 inhibited the growth of colon 
      cancer cells by binding to the 110kDa GP receptor. Inhibition of growth by MLS128 
      did not appear to affect IGF-IR signaling and instead only affected other growth 
      signaling pathways.
FAU - Zamri, N
AU  - Zamri N
AD  - Department of Applied Biochemistry, Tokai University School of Engineering, 
      Hiratsuka, Kanagawa, Japan.
FAU - Masuda, N
AU  - Masuda N
FAU - Oura, F
AU  - Oura F
FAU - Yajima, Y
AU  - Yajima Y
FAU - Nakada, H
AU  - Nakada H
FAU - Fujita-Yamaguchi, Y
AU  - Fujita-Yamaguchi Y
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Japan
TA  - Biosci Trends
JT  - Bioscience trends
JID - 101502754
RN  - 0 (Antibodies, Monoclonal)
RN  - 0 (Antigens, Tumor-Associated, Carbohydrate)
RN  - 0 (Tn antigen)
RN  - EC 2.7.10.1 (Receptor, IGF Type 1)
SB  - IM
MH  - Antibodies, Monoclonal/*immunology/*pharmacology
MH  - Antigens, Tumor-Associated, Carbohydrate/*immunology
MH  - Blotting, Western
MH  - Cell Line, Tumor
MH  - Cell Proliferation/drug effects
MH  - Colonic Neoplasms
MH  - HT29 Cells
MH  - Humans
MH  - Receptor, IGF Type 1/*immunology
MH  - Signal Transduction/drug effects
EDAT- 2013/01/23 06:00
MHDA- 2013/06/26 06:00
CRDT- 2013/01/23 06:00
PHST- 2013/01/23 06:00 [entrez]
PHST- 2013/01/23 06:00 [pubmed]
PHST- 2013/06/26 06:00 [medline]
AID - 609 [pii]
PST - ppublish
SO  - Biosci Trends. 2012 Dec;6(6):303-12.