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.
The IC<sub>50</sub> values varied from 0.36 μM (against MCF7 cells) to 5.65 μM (towards colon carcinomaDLD-1 cells) for 9, from 9.78 μM (against MCF7 cells) to 67.68 μM (against HepG2 cells) for 13 and 0.18 μM (towards HepG2 cells) to 72 μM (towards Caco-2 cells) for the reference drug, doxorubicin.
We examined the anti-proliferative effect of miR-143#12 and the mechanism in human colon cancerDLD-1 cell (G13D) and other cell types harboring K-Ras mutations.
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 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.
The effects of fucoidan from the brown alga <i>Fucus evanescence</i> on the activity of alpha-NaGalase in human colon carcinomaDLD-1 cells and on the biosynthesis of this enzyme were investigated.
Furthermore, this method could detect multiple TFs in human colon cancerDLD-1 cells and reflect the variation in their cellular levels after stimulation.
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.
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.
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.
Global shotgun proteomic analysis of isogenic DLD-1 and RKO colon cancer cell lines expressing mutant and wild type KRAS or BRAF, respectively, failed to identify significant differences (at least 2-fold) in metabolic protein abundance.
To discover the small molecule inhibitors of the Wnt/β-catenin pathway, we conducted high-throughput screening in APC-mutant colon cancerDLD-1 cells using a transcriptional reporter assay, which identified a selective Wnt/β-catenin pathway inhibitor, K-756.
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 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.
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.
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.
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.
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.