To determine the antitumor efficacy, a syngeneic tumor model in BALB/c mice was created using colon cancerCT26.WT cells, and a xenogeneic tumor model was created in nude mice using the human colon cancer SW480 cell line.Mice were treated with schedule 1.
The aim of this study was to investigate the effects of catalpol on the proliferation, growth, invasion, tumor angiogenesis and inflammation of CT26colon cancer in vitro and in vivo.
Oral vaccination of T-MPs generated potent inhibitory effect against the growth of B16 melanoma and CT26colon cancer in mice, which required both T cell and DC activation.
MATERIAL AND METHODS We evaluated the expression of TNF-α in 108 human colon cancer tissue samples and 2 colon cancer cell lines (CT26 and HCT116), and analyzed its prognostic values.
In conclusion, the antitumor effect of ZOL on CT26colon cancer cells in vitro is achieved by apoptosis induction and autophagy regulation, resulting in inhibition of cell proliferation.
Linoleic acid (LA; C-18, n-6 unsaturated fatty acid) and elaidic acid (EA; C-18, trans acid), both known to affect colon carcinogenesis and cancer progression, were administered by gavage to BALB/c mice, which were inoculated with CT26 syngeneic colon cancer cells in the back.
Murine macrophage Raw264.7 cells expressing an enhanced firefly luciferase (Raw/effluc) and murine colon cancer CT26 cells coexpressing Rluc and mCherry (CT26/Rluc-mCherry, CT26/RM) were established.
In this study, transfection of VP3 and silencing of CD147 genes was achieved through the treatment of tumors with pVIVO1-GFP/VP3 (VP3), psiRNA-CD147/2 (shCD147/2), and their combination of CT26colon cancer cell-induced in mice.
Here, we revealed that the serpin Spn4 from Drosophila melanogaster inhibits the activity of all the PCs found in the constitutive secretory pathway and represses the metastatic potential of the colon cancer cells HT-29 and CT-26.
Adenovirus-mediated TIMP3 transduction in CT26colon cancer model demonstrated multiple effects to arrest cancer cell growth and induced massive apoptosis.
The in vivo capability of 2-14 to sensitize colon cancer cells to TRAIL-induced apoptosis was evaluated in a syngenic colon cancer model in which CT26-derived grafts were induced in mice.
Finally, Rhox5 knockdown by small hairpin RNA (shRNA) in CT26colon cancer decreased cell proliferation and migration in vitro and tumor growth in vivo .
Various doses of I-131 (75, 300, 600, 1,200, and 2,400 microCi/5 mL) were incubated with hNIS-expressing colon cancer (CT26/hNIS) and parental cells (CT26), and numbers of MHC class I and Fas-expressing cells were determined by fluorescence-activated cell sorting (FACS).
In the highly metastatic CT26 murine colon cancer cell line, which expresses endogenous TrkC, silencing TrkC expression by small interfering RNA significantly enhanced BMP-2-induced Smad1 phosphorylation and restored BMP-2 growth inhibitory activity.
To evaluate the clinical efficacy of monoclonal antibody (mAb) 3E10 Fv antibody-mediated p53 protein therapy, an Fv-p53 fusion protein produced in Pichia pastoris was tested on CT26.CL25 colon cancer cells in vitro and in vivo in a mouse model of colon cancer metastasis to the liver.
We also used Foxm1 small interfering RNA-depleted human DLD1 and mouse CT26colon cancer cell lines to examine DNA replication and anchorage-independent growth.
In this study, we investigated the antitumor effect of in vivo gene transfer of CD40L to tumor cells using an adenoviral vector (AdCMVmCD40L) in a murine CT-26colon cancer model.