Implication of the Galectin-3 in colorectal cancer development (about 325 Tunisian Patients)

Arfaoui-Toumi, A.; Kria-BenMahmoud, L.; Benhmida, Mohamed; Khalfallah, Mohamed Tahar; Regaya-Mzabi, S.; Bouraoui, Saâdia

doi:10.1684/bdc.2010.1032

Cited by 20 publications

(11 citation statements)

References 29 publications

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“…Moreover, the plasma levels of galectin-1 were shown to be significantly higher in RCC patients when compared to healthy controls [15]. Galectin-3 had also previously been associated with several cancer entities, such as small-cell lung cancer, gastric and colorectal cancer [22-24]. Previous studies were able to show an up-regulation of galectin-3 in RCC [25,26].…”

Section: Discussionmentioning

confidence: 99%

Galectin-1 and Galectin-3 mRNA expression in renal cell carcinoma

et al. 2014

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BackgroundGalectins are known to regulate cell differentiation and growth as well as cell adhesion and apoptosis. Galectins have been discussed as possible prognosticators for survival in renal cell cancer (RCC) and other urological tumors. They might also play an emerging role as possible new marker-proteins for RCC. In this study, we analyzed the expression of galectin-1 and galectin-3 mRNA in order to further investigate their clinical significance in RCC.MethodsTissue samples were obtained from 106 patients undergoing surgery for RCC. The expression of galectin-1 and galectin-3 mRNA in normal kidney and corresponding cancer tissue was analyzed using quantitative real time PCR. Differences in expression levels of paired tissue samples were assessed using paired two-sample tests. Associations of relative mRNA expression levels in tumor tissues with clinical findings were analyzed using univariate logistic regression.ResultsThe expression of galectin-1 (p < 0.001) and -3 (p < 0.001) mRNA were significantly higher in RCC when compared to the adjacent normal kidney tissue. For clear cell RCC, an association of male gender with higher galectin-1 and galectin-3 mRNA expression (p = 0.054, p = 0.034) was detected. For all RCCs, galectin-1 mRNA expression failed to show a significant association with advanced disease as well as a higher rate of lymph node metastases (p = 0.058, p = 0.059).ConclusionThe mRNA expression of galectin-1 and galectin-3 is significantly increased in RCC cancer tissue. The higher mRNA expression in tumor tissue of male patients raises the question of a functional connection between galectins and the higher prevalence of RCC in men. Associations with advanced disease might lead to new ways of identifying patients at higher risk of recurrent disease and might even facilitate early metastasectomy with curative intent.

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Section: Discussionmentioning

confidence: 99%

Galectin-1 and Galectin-3 mRNA expression in renal cell carcinoma

et al. 2014

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“…Reduction of galectin‐3 expression using anti‐sense technology before tumor cell inoculation in mice is associated with a marked reduction in liver colonization and spontaneous metastasis by the high‐metastasing colonic adenocarcinoma cells LSLiM6 and HM7 whereas increase of galectin‐3 expression is associated with an increase in liver metastasis by the low‐metastasizing colonic LS174T cells 68. Higher galectin‐3 expression in colon cancer patients is associated with increased risk of metastasis and has been suggested to be a useful prognostic marker 69, 70…”

Section: Galectins In Cancer Cell Adhesion and Metastasismentioning

confidence: 99%

The role of galectins in colorectal cancer progression

Barrow

Rhodes

2011

Intl Journal of Cancer

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Galectins constitute a family of 15 mammalian galactoside-binding proteins that share a consensus amino acid sequence in their carbohydrate binding sites. They are multi-functional molecules and are expressed widely in human tissues. Four galectins: galectin 21, 23, 24 and 28 are expressed in the human colon and rectum and their expressions show significant changes during colorectal cancer development and metastasis. These changes in galectin expression correlate with alterations in cancer cell growth, apoptosis, cell-cell and cell-matrix interactions and angiogenesis. This review summaries current knowledge of the expression and roles of these galectins in the progression of human colorectal cancer and discusses the relevance of galectins and their ligands as potential therapeutic targets for cancer treatment.The galectins are a family of 15 mammalian galactosidebinding proteins that share a consensus amino acid sequence in their carbohydrate recognition domains (CRDs). 1 On the basis of their structural differences, members of the galectin family are classified into three subgroups: the prototype, chimera-type and tandem-repeat type. The prototype galectins include galectin-1, À2, À5, À7, À10, À11, À13, À14 and À15. They contain a single CRD in their polypeptide sequences and are often identified as non-covalently linked homodimers. The chimera-type galectin, which has only one member (galectin-3), is composed of a non-lectin domain linked to a CRD and can precipitate as a pentamer. The tandem-repeat-type galectins include galectin-4, À6, À8, À9 and À12 and members of this subgroup of galectins contain two CRDs in a single polypeptide chain and these two CRDs are often different from each other. All galectins are bivalent or multivalent molecules in physiological or pathological conditions as a result either of the presence of two CRDs within a single polypeptide chain or by polymerization, and are able to form arrays and lattice structures on the cell surface following binding to their carbohydrate ligands. 2 Expression of Galectins in Normal and Cancerous Human Colon and RectumIn the normal human colon and rectum, four galectins, galectin-1, À3, À4 and À8, are expressed 3-6 (Table 1).Galectin-1 is expressed weakly in normal colonic epithelium but its expression is increased in inflammation and cancer. Over expression of galectin-1 correlates with increased metastasis of colorectal cancer. 12 Immunohistochemistry reveals galectin-1 expression in 12% of normal colonic mucosa, 40% of adenomas and 84% of carcinomas. 4 Galectin-1 expression is not confined to the epithelium and 91% of adenocarcinomas and 33% of mucinous adenocarcinomas also show strong stromal galectin-1 expression. 4 Galectin-3, one of the most extensively studied galectins, is widely expressed in the human gastrointestinal tract including the colon and rectum. Normal colonic mucosa shows strong nuclear expression of galectin-3. The cells at the base of the crypt have a weak or negative galectin-3 expression, and the intensity of nuclear galecti...

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“…Galactin-3 (gal-3; MAC2) is a β-galactoside-binding lectin present in the nucleus and cytoplasm; it has been linked to the behavior of colon cancer cells with down-regulation noted with tumor invasion and progression [27] , [28] , [29] . In contrast, others noted increased gal-3 staining with progression [30] , [31] .…”

Section: Resultsmentioning

confidence: 99%

Characterization of Dextran Sodium Sulfate-Induced Inflammation and Colonic Tumorigenesis in Smad3−/− Mice with Dysregulated TGFβ

et al. 2013

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There are few mouse models that adequately mimic large bowel cancer in humans or the gastrointestinal inflammation which frequently precedes it. Dextran sodium sulphate (DSS)-induces colitis in many animal models and has been used in combination with the carcinogen azoxymethane (AOM) to induce cancer in mice. Smad3 −/− mice are deficient in the transforming growth factor beta (TGFβ) signaling molecule, SMAD3, resulting in dysregulation of the cellular pathway most commonly affected in human colorectal cancer, and develop inflammation-associated colon cancer. Previous studies have shown a requirement for a bacterial trigger for the colitis and colon cancer phenotype in Smad3−/− mice. Studies presented here in Smad3−/− mice detail disease induction with DSS, without the use of AOM, and show a) Smad3 −/− mice develop a spectrum of lesions ranging from acute and chronic colitis, crypt herniation, repair, dysplasia, adenomatous polyps, disseminated peritoneal adenomucinosis, adenocarcinoma, mucinous adenocarcinoma (MAC) and squamous metaplasia; b) the colon lesions have variable galactin-3 (Mac2) staining c) increased DSS concentration and duration of exposure leads to increased severity of colonic lesions; d) heterozygosity of SMAD3 does not confer increased susceptibility to DSS-induced disease and e) disease is partially controlled by the presence of T and B cells as Smad3 −/− Rag2 −/− double knock out (DKO) mice develop a more severe disease phenotype. DSS-induced disease in Smad3 −/− mice may be a useful animal model to study not only inflammation-driven MAC but other human diseases such as colitis cystica profunda (CCP) and pseudomyxomatous peritonei (PMP).

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Implication of the Galectin-3 in colorectal cancer development (about 325 Tunisian Patients)

Cited by 20 publications

References 29 publications

Galectin-1 and Galectin-3 mRNA expression in renal cell carcinoma

Galectin-1 and Galectin-3 mRNA expression in renal cell carcinoma

The role of galectins in colorectal cancer progression

Characterization of Dextran Sodium Sulfate-Induced Inflammation and Colonic Tumorigenesis in Smad3−/− Mice with Dysregulated TGFβ

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