LECT2-knockout (KO) mice and NOD/SCID/IL2rgnull (NSG) mice were respectively used to investigate the effects of LECT2 on the tumorigenicity and metastasis of murine (Lewis lung carcinoma, LLC) and human (HCC827) lung cancer cells.
<b>Methods:</b> In our study, a Lewis lung carcinoma transplant mouse model was established and treated with the recombinant human [rh]-endostatin, Endostar, combined with gemcitabine at different sequences.
Rh-endostatin could normalize the tumor vasculature and microenvironment in Lewis lung carcinoma probably via modulation of the balance between vascular endothelial growth factor-A and thrombospondin-1.
In the present work, we tested the activity of two non-replicative herpes simplex virus (HSV)-1-based vectors, encoding human endostatin::angiostatin or endostatin::kringle5 fusion proteins in combination with HSV-1 thymidine kinase (TK) molecule, on endothelial cells (ECs) and Lewis lung carcinoma (LLC) cells.
In the present study, a unique plasmid vector for the mouse endostatin gene, pXLG-mEndo, was constructed and evaluated with and without radiation using the Lewis lung carcinoma (LLC) cell line.
The data showed that the ectopic ES in circulation expressed by intramuscular administration of formulated ES-encoding plasmid DNA significantly suppressed primary tumor growth and lung metastasis in LLC-bearing C57/BL mice.
In Lewis lung carcinoma (LLC) and CMT167 models, dual inhibition of COX-2 and EGFR by melafolone promoted survival, tumor growth inhibition, and vascular normalization, and ameliorated CD8<sup>+</sup> T-cell suppression, accompanied by the downregulation of transforming growth factor-<i>β</i> (TGF-<i>β</i>), vascular endothelial growth factor (VEGF), and PD-L1 in the tumor cells.
The contribution of the COX-2 in IH-induced enhanced tumor malignancy was assessed using celecoxib as a COX-2 specific inhibitor in a murine model of OSA bearing Lewis lung carcinoma (LLC1) tumors.
The combination of bezafibrate plus anti-PD-L1 reached synergistic tumoricidal effect in LLC xenograft mouse models, even though bezafibrate alone had no effect on tumor growth.
We also detected downregulation of PD-L1 in FXR-overexpressing Lewis lung carcinoma (LLC) mouse syngeneic models, indicating an FXR<sup>high</sup>PD-L1<sup>low</sup> subtype in which FXR suppresses tumor-infiltrating immune cells.
Male C57BL/6J mice were injected with 1X106 Lewis Lung Carcinoma (LLC) cells dissolved in 100 µL PBS and cancer was allowed to develop for 1, 2, 3, or 4 weeks.
In Lewis lung carcinoma (LLC) and CMT167 models, dual inhibition of COX-2 and EGFR by melafolone promoted survival, tumor growth inhibition, and vascular normalization, and ameliorated CD8<sup>+</sup> T-cell suppression, accompanied by the downregulation of transforming growth factor-<i>β</i> (TGF-<i>β</i>), vascular endothelial growth factor (VEGF), and PD-L1 in the tumor cells.
In Lewis lung carcinoma (LLC) and CMT167 models, dual inhibition of COX-2 and EGFR by melafolone promoted survival, tumor growth inhibition, and vascular normalization, and ameliorated CD8<sup>+</sup> T-cell suppression, accompanied by the downregulation of transforming growth factor-<i>β</i> (TGF-<i>β</i>), vascular endothelial growth factor (VEGF), and PD-L1 in the tumor cells.
Male C57BL/6J mice were injected with 1X106 Lewis Lung Carcinoma (LLC) cells dissolved in 100 µL PBS and cancer was allowed to develop for 1, 2, 3, or 4 weeks.
Here, we report on the in vivo characterization of the anti-cancer activity of IL2-F8-TNF<sup>mut</sup> in four immunocompetent murine models of cancer, CT26, WEHI-164, F9 teratocarcinoma and Lewis lung carcinoma (LLC), using the product alone or in combination with a monoclonal antibody specific to murine PD-L1.
RNA sequencing of gastrocnemius muscle samples showed widespread alterations in LLC compared with PBS animals with largest differences seen in 4 wk LLC, suggesting extensive transcriptomic alterations concurrent to muscle wasting.
Lewis lung carcinoma (LLC) was injected into the hind flank of C57BL6/J mice at 8 weeks age with tumour allowed to develop for 1, 2, 3, or 4 weeks and compared with PBS injected control.
Lewis lung carcinoma (LLC) was injected into the hind flank of C57BL6/J mice at 8 weeks age with tumour allowed to develop for 1, 2, 3, or 4 weeks and compared with PBS injected control.
RNA sequencing of gastrocnemius muscle samples showed widespread alterations in LLC compared with PBS animals with largest differences seen in 4 wk LLC, suggesting extensive transcriptomic alterations concurrent to muscle wasting.
Using the Lewis lung carcinoma (LLC) model, we show that tumor growth induces a progressive increase in peripheral inflammation as observed by elevated interleukin-6 (IL-6).