The ectopic expression of mimic miR-31 showed significant 5-FU resistance in the parental DLD-1 cells, while anti-miR-31 caused significant growth inhibition in DLD/F cells; that is, 5-FU-resistant colon cancer cell line DLD-1 under exposure to 5-FU.
Furthermore, this method could detect multiple TFs in human colon cancerDLD-1 cells and reflect the variation in their cellular levels after stimulation.
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.
alpha-Mangostin, a xanthone from the pericarps of mangosteen (Garcinia mangostana Linn.), was evaluated for in vitro cytotoxicity against human colon cancerDLD-1 cells.
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.
Here, we detected its effects on DLD-1 and SW480 (two human colon cancer cell lines) and investigated the dynamic relationship between the 78-kDa glucose-regulatory protein (GRP78) and the phosphoinositide 3-kinase (PI3K)/Akt pathway.
In vitro analyses showed that ectopic expression of miR-215 decreases viability and migration, increases apoptosis and promotes cell cycle arrest in DLD-1 and HCT-116 colon cancer cell lines.
Combination treatment of human colon cancerDLD-1 cells with 2 of these compounds, each at its IC20 concentration, induced apoptosis by stimulating both intrinsic and extrinsic apoptosis signaling pathways.
Gated MSNs are nontoxic to colon cancerDLD-1 cells, and ATTO 430LS dye delivered correlated with the amount of Le<sup>x</sup> antigen overexpressed at the DLD-1 cell surface.
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.
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.
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.
DLD-1 and SW480 colon cancer cell lines were transfected with vectors expressing transgenes or small hairpin RNAs and incubated with recombinant PGE<sub>2</sub>, with or without pharmacologic inhibitors of signaling proteins, and analyzed by immunoblot, immunofluorescence, quantitative reverse-transcription polymerase chain reaction, transcriptional reporter, and proliferation assays.
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.
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.
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.
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.