PMID- 8306524
OWN - NLM
STAT- MEDLINE
DCOM- 19940317
LR  - 20200304
IS  - 0262-0898 (Print)
IS  - 0262-0898 (Linking)
VI  - 12
IP  - 2
DP  - 1994 Mar
TI  - Desialylation of metastatic human colorectal carcinoma cells facilitates binding 
      to Kupffer cells.
PG  - 108-16
AB  - Cell surface hypersialylation of human colorectal carcinoma (HCRC) cells 
      correlates with increased metastatic potential after intrasplenic injection, 
      while desialylation with various agents has been shown to inhibit hepatic 
      metastases. In this study we examined the effects of desialylation of HCRC cell 
      lines with a novel intracellular inhibitor of the CMP-sialic acid transport 
      protein (KI-8110). HCRC cells, which are poorly differentiated and poorly 
      metastatic in nude mice (Clone A and MIP-101) were compared to 
      well-differentiated, highly metastatic cells (CX-1 and CCL-235). KI-8110 
      treatment has previously been shown to reduce sialic acid levels in each of these 
      cell lines and to reduce hepatic metastases in CX-1 and CCL-235 cell lines. This 
      study attempts to identify a mechanism by which desialylation inhibits hepatic 
      metastases. After KI-8110 treatment, in vitro adhesion assays were performed with 
      each cell line to examine binding to Kupffer cells and the extracellular matrix 
      protein fibronectin. Binding of Clone A, CX-1, and CCL-235 to Kupffer cells was 
      significantly increased after KI-8110 treatment. Desialylation had no significant 
      effect on binding of HCRC cell lines to fibronectin. While the metastatic cascade 
      involves many complex interactions, the cytotoxic effects of Kupffer cells in the 
      hepatic sinusoid are known to be an important mechanism of host defense against 
      tumor cells. Cell surface sialic acids may well mask Kupffer cell binding to HCRC 
      cells, preventing their cytotoxic effects and enhancing the metastatic potential 
      of circulating tumor cells.
FAU - Petrick, A T
AU  - Petrick AT
AD  - Department of Surgery, Deaconess Hospital, Harvard Medical School, Boston.
FAU - Meterissian, S
AU  - Meterissian S
FAU - Steele, G Jr
AU  - Steele G Jr
FAU - Thomas, P
AU  - Thomas P
LA  - eng
GR  - CA44583/CA/NCI NIH HHS/United States
GR  - CA44704/CA/NCI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - Netherlands
TA  - Clin Exp Metastasis
JT  - Clinical & experimental metastasis
JID - 8409970
RN  - 0 (Glycosides)
RN  - 0 (Sialic Acids)
RN  - 80681-73-8 (KI 8110)
RN  - EC 2.4.99.- (Sialyltransferases)
RN  - GZP2782OP0 (N-Acetylneuraminic Acid)
RN  - WHI7HQ7H85 (Uridine)
SB  - IM
MH  - Animals
MH  - Colorectal Neoplasms/*metabolism/pathology
MH  - Glycosides/metabolism/pharmacology
MH  - Humans
MH  - Kupffer Cells/*metabolism
MH  - Liver Neoplasms/secondary
MH  - Mice
MH  - Mice, Nude
MH  - N-Acetylneuraminic Acid
MH  - Neoplasm Metastasis
MH  - Sialic Acids/metabolism
MH  - Sialyltransferases/metabolism
MH  - Tumor Cells, Cultured
MH  - Uridine/analogs & derivatives/metabolism/pharmacology
EDAT- 1994/03/01 00:00
MHDA- 2001/03/28 10:01
CRDT- 1994/03/01 00:00
PHST- 1994/03/01 00:00 [pubmed]
PHST- 2001/03/28 10:01 [medline]
PHST- 1994/03/01 00:00 [entrez]
AID - 10.1007/BF01753977 [doi]
PST - ppublish
SO  - Clin Exp Metastasis. 1994 Mar;12(2):108-16. doi: 10.1007/BF01753977.