To define the inhibitory and pro-apoptotic effects of the two PI3K inhibitors BEZ235 and BKM120 in three human colon cancer (HT-29, HCT-116 and DLD-1) and three gastric cancer (NCI-n87, AGS and MKN-45), cell lines with different PIK3CA gene mutation status were used.
In addition, DLD-1 human colon cancer cells were employed as a cellular model to study the role of CK2α on cell growth, and the expression of CK2α in DLD-1 cells was inhibited by using siRNA technology.
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.
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.
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.
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.
alpha-Mangostin, a xanthone from the pericarps of mangosteen (Garcinia mangostana Linn.), was evaluated for in vitro cytotoxicity against human colon cancerDLD-1 cells.
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.
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.
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.
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.
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, the expression of endothelin-1 and endothelin receptors was studied in eight human tumour cell lines: T98G (glioblastoma), IMR-32 and NB69 (neuroblastoma), BeWo (choriocarcinoma), SW-13 (adrenocortical carcinoma), DLD-1 (colonic carcinoma), HeLa (cervical carcinoma) and VMRC-RCW (renal carcinoma).
The epithelial origin of all identified spots was checked in two cell lines Caco-2 and DLD-1 originating from well-differentiated and poorly differentiated colon carcinoma, respectively.
However, when DLD-1 human colon carcinoma cells were transfected with antisense SAG, monolayer growth was significantly inhibited, as shown by a decreased number of stable colonies in the plate after normalization with transfection efficiency.
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.