PMID- 12008042
OWN - NLM
STAT- MEDLINE
DCOM- 20020917
LR  - 20190826
IS  - 0165-2478 (Print)
IS  - 0165-2478 (Linking)
VI  - 82
IP  - 1-2
DP  - 2002 Jun 3
TI  - Possible co-regulation of genes associated with enhanced progression of mammary 
      adenocarcinomas.
PG  - 111-21
AB  - Tumor progression is a multistep process in which alterations in the expression 
      of numerous gene products may give rise to highly malignant cellular variants. In 
      the present study, we analyzed the differential expression of several genes in 
      cellular variants of mammary adenocarcinomas with high or low malignancy 
      potential, which originated in a common ancestor. To assess the generality of our 
      findings, high and low malignancy variants were derived from two different 
      mammary adenocarcinoma cell lines, namely DA3 and CSML cells. Of major importance 
      is the fact that the differences between high- and low-malignancy variants 
      observed in one system of mammary adenocarcinoma cells (DA3 cells) were 
      identically reproduced in the other system of mammary adenocarcinoma cells (CSML 
      cells). The high malignancy variants of tumors both DA3-high and CSML-high 
      (previously called CSML-100), expressed higher levels of factors that induce 
      monocyte migration than the low malignancy DA3-low and CSML-low (previously 
      called CSML-0) variants. In addition, it was found that DA3-high and CSML-high 
      cell variants expressed higher levels of monocyte chemoattractant protein-1 
      (MCP-1), interleukin-6 (IL-6) and matrix metalloproteinases (MMPs) than the low 
      malignancy variants (DA3-low and CSML-low). These results suggest that MCP-1, 
      IL-6 and MMPs potentially contribute to mammary adenocarcinoma progression and 
      that their expression is regulated by a common pathway. The expression of MCP-1, 
      IL-6 and MMPs in both DA3-high and CSML-high cells was up-regulated by tumor 
      necrosis factor alpha (TNFalpha). The fact that TNFalpha exerted similar effects 
      on the expression of these three factors in both cell systems raises the 
      possibility of a coordinated co-regulation of tumor-promoting factors.
FAU - Neumark, E
AU  - Neumark E
AD  - Department of Cell Research and Immunology, George S. Wise Faculty of Life 
      Sciences and The Ela Kodesz Institute for Research on Cancer Development and 
      Prevention, Tel-Aviv University, Tel-Aviv, Israel.
FAU - Cohn, M A
AU  - Cohn MA
FAU - Lukanidin, E
AU  - Lukanidin E
FAU - Witz, I P
AU  - Witz IP
FAU - Ben-Baruch, A
AU  - Ben-Baruch A
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Netherlands
TA  - Immunol Lett
JT  - Immunology letters
JID - 7910006
RN  - 0 (Chemokine CCL2)
RN  - 0 (Interleukin-6)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - EC 3.4.24.- (Matrix Metalloproteinases)
SB  - IM
MH  - Adenocarcinoma/*genetics/metabolism/pathology
MH  - Animals
MH  - Cell Movement
MH  - Chemokine CCL2/biosynthesis
MH  - Disease Progression
MH  - Female
MH  - *Gene Expression Regulation, Neoplastic
MH  - Humans
MH  - Interleukin-6/biosynthesis
MH  - Mammary Neoplasms, Animal/*genetics/metabolism/pathology
MH  - Matrix Metalloproteinases/biosynthesis/genetics
MH  - Mice
MH  - Monocytes/physiology
MH  - Tumor Cells, Cultured
MH  - Tumor Necrosis Factor-alpha/pharmacology
MH  - Up-Regulation
EDAT- 2002/05/15 10:00
MHDA- 2002/09/18 10:01
CRDT- 2002/05/15 10:00
PHST- 2002/05/15 10:00 [pubmed]
PHST- 2002/09/18 10:01 [medline]
PHST- 2002/05/15 10:00 [entrez]
AID - S0165247802000263 [pii]
AID - 10.1016/s0165-2478(02)00026-3 [doi]
PST - ppublish
SO  - Immunol Lett. 2002 Jun 3;82(1-2):111-21. doi: 10.1016/s0165-2478(02)00026-3.