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Expression and functions of galectin-7 in human and murine melanomas.

Biron-Pain K, Grosset AA, Poirier F, Gaboury L, St-Pierre Y - PLoS ONE (2013)

Bottom Line: 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.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.

View Article: PubMed Central - PubMed

Affiliation: INRS-Institut Armand-Frappier, Laval, Québec, Canada.

ABSTRACT
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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Effect of galectin-7 in B16F1 cells on survival and metastasis in lungs.A) Survival curve of C57BL/6 mice injected i.v. with B16F1 transfectant cells overexpressing galectin-7 (□) or controls (♦) (2×105 cells) (n = 8−10). B) Luciferase assay of lungs of C57BL/6 mice sacrificed at 9, 12, 15 or 18 days after the i.v. injection of a mixture of B16F1 luciferase transfectant cells overexpressing galectin-7 (+) or control (–) (n = 3−8). Normal lungs were used as a negative control (T: 0; n = 2). C) Ex vivo imaging of a lung metastasis, as seen in (B), of B16F1 cells overexpressing galectin-7 (iii and v) or control cells (ii and iv) at 9 and 18 days in comparison with control lungs (i).
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pone-0063307-g006: Effect of galectin-7 in B16F1 cells on survival and metastasis in lungs.A) Survival curve of C57BL/6 mice injected i.v. with B16F1 transfectant cells overexpressing galectin-7 (□) or controls (♦) (2×105 cells) (n = 8−10). B) Luciferase assay of lungs of C57BL/6 mice sacrificed at 9, 12, 15 or 18 days after the i.v. injection of a mixture of B16F1 luciferase transfectant cells overexpressing galectin-7 (+) or control (–) (n = 3−8). Normal lungs were used as a negative control (T: 0; n = 2). C) Ex vivo imaging of a lung metastasis, as seen in (B), of B16F1 cells overexpressing galectin-7 (iii and v) or control cells (ii and iv) at 9 and 18 days in comparison with control lungs (i).

Mentions: We next investigated whether galectin-7 could modulate the tumor progression of B16 melanoma cells. For this purpose, we first compared the growth of B16 cells expressing high levels of galectin-7 (B16-G7) with control cells (B16-Srα). Our results showed that mice injected with B16 cells had similar survival rates regardless of galectin-7 expression (26±2.3 days (n = 12) for galectin-7-expressing cells vs. 25.9±3.7 days (n = 12) for controls) (Fig. 6a). This result was observed in independent experiments using either 1×104 or 5×104 cells (data not shown). To study the effect of galectin-7 on melanoma metastasis, we used genetically engineered B16F1 cells overexpressing luciferase. This cell line model facilitates cancer cell detection in target organs with a luciferase assay or the ex vivo bioluminescence imaging of organs. Although we observed a time-dependent increase in the metastatic load in the lung, the number of metastases was similar in mice injected with galectin-7 transfectant cells compared with those injected with control cells (Fig. 6b and 6c).


Expression and functions of galectin-7 in human and murine melanomas.

Biron-Pain K, Grosset AA, Poirier F, Gaboury L, St-Pierre Y - PLoS ONE (2013)

Effect of galectin-7 in B16F1 cells on survival and metastasis in lungs.A) Survival curve of C57BL/6 mice injected i.v. with B16F1 transfectant cells overexpressing galectin-7 (□) or controls (♦) (2×105 cells) (n = 8−10). B) Luciferase assay of lungs of C57BL/6 mice sacrificed at 9, 12, 15 or 18 days after the i.v. injection of a mixture of B16F1 luciferase transfectant cells overexpressing galectin-7 (+) or control (–) (n = 3−8). Normal lungs were used as a negative control (T: 0; n = 2). C) Ex vivo imaging of a lung metastasis, as seen in (B), of B16F1 cells overexpressing galectin-7 (iii and v) or control cells (ii and iv) at 9 and 18 days in comparison with control lungs (i).
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Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC3643947&req=5

pone-0063307-g006: Effect of galectin-7 in B16F1 cells on survival and metastasis in lungs.A) Survival curve of C57BL/6 mice injected i.v. with B16F1 transfectant cells overexpressing galectin-7 (□) or controls (♦) (2×105 cells) (n = 8−10). B) Luciferase assay of lungs of C57BL/6 mice sacrificed at 9, 12, 15 or 18 days after the i.v. injection of a mixture of B16F1 luciferase transfectant cells overexpressing galectin-7 (+) or control (–) (n = 3−8). Normal lungs were used as a negative control (T: 0; n = 2). C) Ex vivo imaging of a lung metastasis, as seen in (B), of B16F1 cells overexpressing galectin-7 (iii and v) or control cells (ii and iv) at 9 and 18 days in comparison with control lungs (i).
Mentions: We next investigated whether galectin-7 could modulate the tumor progression of B16 melanoma cells. For this purpose, we first compared the growth of B16 cells expressing high levels of galectin-7 (B16-G7) with control cells (B16-Srα). Our results showed that mice injected with B16 cells had similar survival rates regardless of galectin-7 expression (26±2.3 days (n = 12) for galectin-7-expressing cells vs. 25.9±3.7 days (n = 12) for controls) (Fig. 6a). This result was observed in independent experiments using either 1×104 or 5×104 cells (data not shown). To study the effect of galectin-7 on melanoma metastasis, we used genetically engineered B16F1 cells overexpressing luciferase. This cell line model facilitates cancer cell detection in target organs with a luciferase assay or the ex vivo bioluminescence imaging of organs. Although we observed a time-dependent increase in the metastatic load in the lung, the number of metastases was similar in mice injected with galectin-7 transfectant cells compared with those injected with control cells (Fig. 6b and 6c).

Bottom Line: 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.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.

View Article: PubMed Central - PubMed

Affiliation: INRS-Institut Armand-Frappier, Laval, Québec, Canada.

ABSTRACT
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.

Show MeSH
Related in: MedlinePlus