A distinctive role for galectin-7 in cancer ?

St‐Pierre, Yves; Campion, Carole G.; Grosset, Andrée-Anne

doi:10.2741/3937

Cited by 24 publications

(24 citation statements)

References 63 publications

(88 reference statements)

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“…Interestingly, Lee et al [63] claimed that the upregulation of galectin-7 expression occurs in a PGE2-dependent manner as a result of the EC-SOD-mediated activation of COX-2, which leads ultimately to the accumulation of pro-apoptotic molecules, such as caspase-3, caspase-9, Bax, and Bcl-Xs. As to the pathological stress conditions, including cancer, it has been suggested that galectin-7 plays a dual role as a result of its ability to mediate apoptosis and cancer suppression via a p53-dependent pathway and to promote cancer progression via NF-jBdependent pathway [64]. Since both p53 and NF-jB belong to stress-induced transcription factors, the corresponding upregulation of galectin-7 should be considered in the context of specific cellular stress responses with differential outcomes, which fits perfectly with the conceptual paradigm of stress-induced selection between cell death or cell survival.…”

Section: Galectin-7mentioning

confidence: 99%

Towards molecular mechanisms regulating the expression of galectins in cancer cells under microenvironmental stress conditions

Timoshenko

2015

Cell. Mol. Life Sci.

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Galectins, a family of soluble β-galactoside-binding proteins, serve as mediators of fundamental biological processes, such as cell growth, differentiation, adhesion, migration, survival, and death. The purpose of this review is to summarize the current knowledge regarding the ways in which the expression of individual galectins differs in normal and transformed human cells exposed to various stimuli mimicking physiological and pathological microenvironmental stress conditions. A conceptual point is being made and grounded that the modulation of galectin expression profiles is a key aspect of cellular stress responses. Moreover, this modulation might be precisely regulated at transcriptional and post-transcriptional levels in the context of non-overlapping transcription factors and miRNAs specific to galectins.

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Section: Galectin-7mentioning

confidence: 99%

Towards molecular mechanisms regulating the expression of galectins in cancer cells under microenvironmental stress conditions

Timoshenko

2015

Cell. Mol. Life Sci.

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“…This abnormally high expression level of galectin-7 is not restricted to breast cancer cells. It is also found in pancreatic cancer cell lines [14], and in esophageal, buccal, and hypopharyngeal squamous cell carcinoma [10,15–17]. Such high levels of galectin-7 in cancer cells are somewhat paradoxical because galectin-7 has generally been considered a pro-apoptotic protein under the control of p53 .…”

Section: Introductionmentioning

confidence: 99%

Expression of Galectin-7 Is Induced in Breast Cancer Cells by Mutant p53

et al. 2013

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Galectin-7 was initially described as a marker of epithelial differentiation expressed in the stratified epithelium of various tissues. Like other members of the galectin family, its expression level is often significantly altered in cancer cells. In breast cancer, its expression is significantly augmented in aggressive molecular subtypes, most notably in estrogen receptor-negative tumors and in cell lines with a basal-like phenotype. Studies using experimental mouse models have further shown high expression of galectin-7 was sufficient to increase the metastatic behavior of poorly metastatic breast cancer cells, rendering them more resistant to apoptosis. This expression pattern in breast cancer cells is unexpected because galectin-7 was originally identified as a p53-induced gene. To address this paradox, we have examined the molecular mechanisms regulating galectin-7 in breast cancer cells. Our results showed that transfection of breast cancer cells with expression vectors encoding mutant p53 was sufficient to induce galectin-7 at both mRNA and protein levels. Doxorubicin treatment of breast cancer cells harboring a mutant p53 also induced galectin-7. This induction was specific since knockdown of endogenous mutant p53 inhibited doxorubicin-induced galectin-7 expression. The p53-induced galectin-7 expression in breast cancer cells correlated with increased NF-κB activity and was inhibited by NF-κB inhibitors, indicating that the ability of mutant p53 to induce galectin-7 was dependent on NF-κB activity. The implication of NF-κB was further supported by data showing that NF-κB bound to the endogenous galectin-7 promoter and that TNFα-induced galectin-7 expression was abolished by NF-κB inhibitors. Taken together, our data provide an explanation to the observed high galectin-7 expression levels in cancer cells and suggest that galectin-7 could be part of a common pathway used by mutant p53 to promote cancer progression.

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“…A number of indications have suggested that galectin-7 may potentially be important in melanoma proliferation, invasion, and metastasis. Like other members of the galectin family, galectin-7 has been shown to either positively or negatively modulate apoptosis and tumor growth [34]. In colon cancer, for example, galectin-7 has an anti-tumorigenic function [15], in contrast to its pro-tumorigenic function reported in lymphoma, breast cancer, squamous cell carcinoma of the tongue and esophagus, and thyroid malignancies [20]-[22], [35]–[37].…”

Section: Discussionmentioning

confidence: 99%

Expression and Functions of Galectin-7 in Human and Murine Melanomas

et al. 2013

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The identification of galectin-7 as a p53-induced gene and its ability to induce apoptosis in many cell types support the hypothesis that galectin-7 has strong antitumor activity. This has been well documented in colon cancer. However, in some cases, such as breast cancer and lymphoma, its high expression level correlates with aggressive subtypes of cancer, suggesting that galectin-7 may have a dual role in cancer progression. In fact, in breast cancer, overexpression of galectin-7 alone is sufficient to promote metastasis to the bone and lung. In the present work, we investigated the expression and function of galectin-7 in melanoma. An analysis of datasets obtained from whole-genome profiling of human melanoma tissues revealed that galectin-7 mRNA was detected in more than 90% of biopsies of patients with nevi while its expression was more rarely found in biopsies collected from patients with malignant melanoma. This frequency, however, was likely due to the presence of normal epidermis tissues in biopsies, as shown our studies at the protein level by immunohistochemical analysis. Using the experimental melanoma B16F1 cell line, we found that melanoma cells can express galectin-7 at the primary tumor site and in lung metastasis. Moreover, we found that overexpression of galectin-7 increased the resistance of melanoma cells to apoptosis while inducing de novo egr-1 expression. Overexpression of galectin-7, however, was insufficient to modulate the growth of tumors induced by the subcutaneous injection of B16F1 cells. It also failed to modulate the dissemination of B16F1 cells to the lung.

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A distinctive role for galectin-7 in cancer ?

Cited by 24 publications

References 63 publications

Towards molecular mechanisms regulating the expression of galectins in cancer cells under microenvironmental stress conditions

Towards molecular mechanisms regulating the expression of galectins in cancer cells under microenvironmental stress conditions

Expression of Galectin-7 Is Induced in Breast Cancer Cells by Mutant p53

Expression and Functions of Galectin-7 in Human and Murine Melanomas

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