The following results were obtained: (1) KAI1 gene expression had no significant effect on in vitro cell growth rate of colon cancer BM314 and DLD-1 cells; (2) Cell aggregation assay showed that KAI1 enhanced the Ca++-independent aggregatability of those colon cancer cells; (3) It was revealed by cell motility and invasion assays that KAI1 suppressed both the motility and in vitro invasiveness of those cells and (4) Furthermore, both the binding to fibronectin and the migration on fibronectin-coated plates of those cells were inhibited by KAI1 expression.
We show here that one allele of the alphaE-catenin (CTNNA1) gene is mutated in the human colon cancer cell family HCT-8, which is identical to HCT-15, DLD-1 and HRT-18.
Cell proliferation of carcinoma cells DLD-1 derived from colon cancer as measured by [3H] thymidine incorporation was drastically reduced in the presence of 4-aminopyridine, an inhibitors of voltage-gated K channel.
In the present study, we constructed a beta-galactosidase reporter gene system in human colon cancerDLD-1 cells, and measured COX-2 promoter-dependent transcriptional activity in the cells.
We identified two sequence variants causing amino acid substitutions in four colon cancer cell lines, a Ser-to-Leu at residue 215 in LS513 and a Leu-to-Met at residue 396 in HCT-8, HCT-15, and DLD-1.
Delivery of these iNOS-expressing cells to tumors formed from human ovarian cancer SKOV-3 cells results in 100% killing, whereas treatment of tumors formed from human colon cancerDLD-1 cells results in 54% killing.
In the present study, we demonstrated synergistic effects between anti-MDM2 antisense oligonucleotides and the clinically used anticancer agent irinotecan, using nude mouse models of human colon cancers (LS174T and DLD-1).
Similar results were observed in RKO, HT-29, and DLDcolon cancer cells demonstrating comparable responses in COX-2-expressing and -nonexpressing colon cancer cell lines.
The aim of this study was to investigate the effects of genistein at concentrations ranging from 0.01 to 100 microM on the polyamine biosynthesis, cell proliferation, and apoptosis in the estrogen receptor-positive DLD-1 human colon cancer cell line.
In order to clarify the mechanisms of estrogenic growth control in colorectal carcinoma, we have investigated the effects of 17beta-estradiol exposure on LDL-R gene expression and its protein, as well as on HMG-CoAR gene expression, its protein as well as enzyme activity in the DLD-1 human colon cancer cell line.
When let-7 low-expressing DLD-1 human colon cancer cells were transfected with let-7a-1 precursor miRNA, which is located at chromosome 9q22.3, the cells underwent significant growth suppression.
The transfection of each precursor miRNA into the cells demonstrated a significant growth inhibition in human colon cancerDLD-1 and SW480 cells, and ERK5 was determined to be the target gene of miRNA 143.
alpha-Mangostin, a xanthone from the pericarps of mangosteen (Garcinia mangostana Linn.), was evaluated for in vitro cytotoxicity against human colon cancerDLD-1 cells.
The present study was designed to investigate the effects of isoflavone genistein exposure at concentrations ranging from 0.01 microM to 50 microM on the LDL receptor and HMGCoA reductase gene expression in the estrogen receptor positive DLD-1 human colon cancer cell line.
Here we show that augmented caveolin-1 expression in cells with low basal levels of this protein, such as human colon cancer (HT29, DLD-1), breast cancer (ZR75), and embryonic kidney (HEK293T) cells reduced COX-2 mRNA and protein levels and beta-catenin-Tcf/Lef and COX-2 gene reporter activity, as well as the production of PGE(2) and cell proliferation.
The expression profiles of human colon cancer cell line DLD-1, its 5-FU-resistant subclone DLD-1/FU and a further 21 types of colon cancer cell lines were compared to identify the novel genes defining the sensitivity to 5-FU and to estimate which population of genes is responsible for 5-FU sensitivity.
The treatment of the colon cancer cell lines SW480 and DLD-1 with paclitaxel resulted in increased activation of the MAPK pathway, which was blocked by PD98059, a MEK inhibitor.
On the contrary, an extracellular signal-regulated protein kinase 5 (ERK5), which was determined to be a target of miR-143 in colon cancerDLD-1 cells, was time-dependently down-regulated at the translational level after the treatment.
Uptake of 3-[125I]iodo-alpha-methyl-L-tyrosine into colon cancerDLD-1 cells: characterization and inhibitory effect of natural amino acids and amino acid-like drugs.