ArticleDigestive diseases and sciences2012
Effects of macrophage metalloelastase on the basic fibroblast growth factor expression and tumor angiogenesis in murine colon cancer.
Article in Digestive diseases and sciences, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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2 citing papers in PubMed, 3 citations in OpenAlex.
- Identification of anti-tumor components from toad venom.Oncology letters · 2017Article
- Predicting cancer-relevant proteins using an improved molecular similarity ensemble approach.Oncotarget · 2016Article
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5 authors at 2 institutions in 1 country.
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Abstract
BACKGROUND AND
aimPrevious studies have shown that overexpression of macrophage metalloelastase (MME) suppresses tumor growth in mice. The purpose of this study was to investigate the effects of MME on basic fibroblast growth factor (bFGF) expression and tumor angiogenesis in murine colon cancer.
methodsMurine CT-26 colon cancer cells stably transfected with MME were inoculated subcutaneously. Reverse-transcriptase polymerase chain reaction (RT-PCR), immunoblotting, and immunohistochemistry were used to explore the bFGF mRNA and protein expression. Immunohistochemical staining of CD34 was used to measure the microvessel density (MVD).
resultsbFGF mRNA levels in tumor tissues of CT-26-EGFP and nontransfected cells were respectively 2.7-fold (0.56 ± 0.063 vs. 0.21 ± 0.042) and 2.5-fold (0.53 ± 0.066 vs. 0.21 ± 0.042) higher than that in tumors of CT-26-EGFP-MME cells (p < 0.01). bFGF protein levels exhibited a similar trend. Tumors of CT-26-EGFP-MME cells demonstrated a lower microvessel density (9.35 ± 2.79) than control tumors of CT-26-EGFP cells (22.85 ± 3.80) and nontransfected cells (23.45 ± 4.49) (p < 0.001).
conclusionsWe found that expression of MME inversely correlates with the expression of bFGF and tumor angiogenesis in a model of murine colon cancer. These data indicate that manipulation of MME expression could be a novel modality approach to colon cancer therapy.
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