Prognostic Values of Galectin-3 and the Macrophage Migration Inhibitory Factor (MIF) in Human Colorectal Cancers

Legendre, Hugues; Decaestecker, Christine; Nagy, Nathalie; Hendlisz, Alain; Schüring, Max-Peter; Salmon, Isabelle; Gabius, Hans‐Joachim; Pector, Jean Claude; Kiss, Róbert

doi:10.1097/01.mp.0000068235.45178.c1

Cited by 88 publications

(72 citation statements)

References 51 publications

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“…We did, however, not observe significant differences in the intensity of expression between lowand high-grade tumours and not in dependence on the disease-free survival, although a prolonged disease-free survival was accompanied by a slight, statistically non-significant reduction in the mean intensity of expression (1.43) as compared to metastasis developing concomitantly with the primary tumour (mean intensity: 1.73). Other studies revealed either similar results or reported upregulation of galectin-3 expression during tumour progression (Andre et al, 1999;Nakamura et al, 1999;Legendre et al, 2003Endo et al, 2005). Particularly one of the latter studies performed a highly sophisticated quantitation of galectin-3 expression .…”

Section: Discussionsupporting

confidence: 66%

C4.4A as a candidate marker in the diagnosis of colorectal cancer

et al. 2007

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C4.4A is a member of the Ly-6 family with restricted expression in non-transformed tissues. C4.4A expression in human cancer has rarely been evaluated. Thus, it became important to explore C4.4A protein expression in human tumour tissue to obtain an estimate on the frequency of expression and the correlation with tumour progression, the study focusing on colorectal cancer. The analysis of C4.4A in human tumour lines by western blot and immunoprecipitation using polyclonal rabbit antibodies that recognize different C4.4A epitopes revealed C4.4A oligomer and heavily glycosylated C4.4A isoform expression that, in some instances, inhibited antibody binding and interaction with the C4.4A ligand galectin-3. In addition, tumour cell lines released C4.4A by vesicle shedding and proteolytic cleavage. C4.4A was expressed in over 80% of primary colorectal cancer and liver metastasis with negligible expression in adjacent colonic mucosa, inflamed colonic tissue and liver. This compares well with EpCAM and CO-029 expression in over 90% of colorectal cancer. C4.4A expression was only observed in about 50% of pancreatic cancer and renal cell carcinoma. By de novo expression in colonic cancer tissue, we consider C4.4A as a candidate diagnostic marker in colorectal cancer, which possibly can be detected in body fluids.

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Section: Discussionsupporting

confidence: 66%

C4.4A as a candidate marker in the diagnosis of colorectal cancer

et al. 2007

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“…Moreover, MIF was identified as a miR-451 target with the bioinformatic prediction program miRBase Targets. 9 We decided to study MIF further, as the overexpression of MIF has been observed in several human neoplasms (31,32), including gastric (33) and colorectal cancer (34), and has been shown to exert effects on a variety of cell types by regulating diverse biological processes. The observed effects include inflammation, immune regulation, physiologic and pathophysiologic neovascularization, and cell replication.…”

Section: Resultsmentioning

confidence: 99%

microRNA-451 Regulates Macrophage Migration Inhibitory Factor Production and Proliferation of Gastrointestinal Cancer Cells

Bandrés¹,

Bitarte²,

Arias

et al. 2009

Clinical Cancer Research

312

246

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Purpose: microRNAs (miRNA) are small RNAs that function as post-transcriptional regulators of gene expression. Recent evidence has shown that some miRNAs can act as oncogenes or tumor suppressors. This study was conducted to evaluate the potential association of miRNA expression with clinical outcome in patients with gastric cancer. Experimental Design: Expression of 250 human mature miRNAs was measured by real-time PCR on paraffin-embedded tumor samples of 21 patients with gastric cancer stage III uniformly treated with surgical resection followed by chemoradiation. We identified the miRNAs correlated with disease-free and overall survival times, and the results were evaluated including 24 other patients. In vitro cell proliferation and radiosensitivity studies were done to support clinical data. Results:The results revealed that down-regulation of miR-451was associated with worse prognosis. miR-451 was detected by in situ hybridization in epithelial cells and showed decreased expression in gastric and colorectal cancer versus nontumoral tissues. Overexpression of miR-451in gastric and colorectal cancer cells reduced cell proliferation and increased sensitivity to radiotherapy. Microarray and bioinformatic analysis identified the novel oncogene macrophage migration inhibitory factor (MIF) as a potential target of miR-451. In fact, overexpression of miR451down-regulated mRNA and protein levels of MIF and decreased expression of reporter genes with MIF target sequences. Moreover, we found a significant inverse correlation between miR451and MIF expression in tumoral gastric biopsies. Conclusions: These findings support the role of miR-451as a regulator of cancer proliferation and opennew perspectives for the development of effective therapies for chemoradioresistant cancers.

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“…It is a unique cytokine affecting multiple processes fundamental to tumorigenesis (Bach et al, 2009). In addition, MIF has prognostic value in human colorectal cancer because its expression correlates with aggressiveness of the cancer (Legendre et al 2003). MT2A gene belongs to the metallothionein families, which are important for metal ion homeostasis.…”

Section: Discussionmentioning

confidence: 99%

eIF3m expression influences the regulation of tumorigenesis-related genes in human colon cancer

Hong

et al. 2010

Oncogene

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Abnormal regulation of gene expression is essential for tumorigenesis. Recent studies indicate that regulation of oncogene expression and neoplastic transformation are controlled by subunits of eukaryotic translation initiation factors (eIFs). Here we focused on eIF3 performing a pivotal role in protein synthesis and the differential expression of its subunits in cancer. The most uncharacterized non-core subunit eIF3m was confirmed to be highly expressed in human cancer cell lines and colon cancer patient tissues. By expression silencing with eIF3m-specific small interfering RNA (siRNA), we confirmed that eIF3m influences cell proliferation, cell cycle progression and cell death in human colon cancer cell line HCT-116. Using a ribonomics approach, we identified a subset of elF3m-influenced genes and showed that the expression of two highly represented tumorigenesis-related genes, MIF and MT2, were affected by eIF3m at the mRNA level. We also confirmed eIF3m-dependent regulation of MT2A downstream molecule CDC25A, which is necessary for cell cycle progression in HCT-116 cells. These results suggest that eIF3m mediates regulation of tumorigenesis-related genes in human colon cancer. Further investigations on tumorigenesis-related genes and their regulation by eIFs will provide clues for designing targeted therapy for cancer.

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Prognostic Values of Galectin-3 and the Macrophage Migration Inhibitory Factor (MIF) in Human Colorectal Cancers

Abstract: In conclusions, MIF and galectin-3 expression levels in colorectal tumors are related to their levels of biological aggressiveness. These markers could be used to identify patients at risk, for whom more aggressive adjuvant therapy seems to be indicated.

Cited by 88 publications

References 51 publications

C4.4A as a candidate marker in the diagnosis of colorectal cancer

C4.4A as a candidate marker in the diagnosis of colorectal cancer

microRNA-451 Regulates Macrophage Migration Inhibitory Factor Production and Proliferation of Gastrointestinal Cancer Cells

eIF3m expression influences the regulation of tumorigenesis-related genes in human colon cancer

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