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.
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.
In the current study, we established a TRAIL-resistant human colon cancerDLD-1 cell line to clarify the mechanisms of TRAIL-resistance and developed agents to cancel its machinery.
Aneuploid DLD-1 and HCT-15 cell lines independently derived from a colon carcinoma by two researchers lacked a common marker chromosome or a concurrent numerical change.
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.
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.
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.
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 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.
We knocked down fascin1 expression with shRNA retrovirally transduced into a DLD-1 colon cancer and L929 fibroblast-like cell lines and used luciferase reporter assays and co-immunoprecipitation to identify fascin1 targets.
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.
Taken together, culturing DLD-1 cells in serum-free medium enriches CSCs and the expression of KLF4 is essential for the characteristics of CSCs in DLD-1; thus KLF4 can be a potential therapeutic target for treating colon cancer.
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.
The parent DLD-1 human colon carcinoma cell line and its two cloned subpopulations provide material for the study of various aspects and implications of human cancer cell heterogeneity.
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.
Literatures support potent anticancer activity of napthoquinone derivatives in human colon cancer, present study evaluates the effect and mechanism of LS on chemical induced colon cancerous rats and human colon cancerDLD-1 cells, the study was supported by endoscopy, histological and immunohistochemistry analysis.
We validated Gn binding to MSI1 using surface plasmon resonance, nuclear magnetic resonance, and cellular thermal shift assay, and tested the effects of Gn on colon cancer cells and colon cancerDLD-1 xenografts in nude mice.
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 examined the effect of differentiation-inducing factor-3 (DIF-3), a monochlorinated metabolite of DIF-1 that is also produced by D. discoideum, on human colon cancer cell lines HCT-116 and DLD-1.
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.