Dataset Information

Quantitative proteomic study of two cervical cancer cell lines upon re-expression of Galectin 7

ABSTRACT: Galectin-7 expression was found to be strongly reduced in cervical cancer cell lines. The same tumor cell lines in which Galectin-7 was ectopically expressed exhibited significant decrease in their tumorigenic capacity in vitro and in vivo. The proteomic changes in the cervical cancer cell lines HeLa and SiHa after Galectin-7 re-expression were here quantified by SILAC.

INSTRUMENT(S): Q Exactive

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Siha Cell, Hela Cell

DISEASE(S): Cervix Carcinoma

SUBMITTER: Jana Klimentova

LAB HEAD: Bladimiro Rincon-Orozco

PROVIDER: PXD001806 | Pride | 2016-09-28

REPOSITORIES: Pride

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Dataset's files

Source:

			Action	DRS
	08112014_100_JK_6-2014-BRO_SiHa1_fr14-16.raw	Raw
	08112014_101_JK_6-2014-BRO_SiHa1_fr16-18.raw	Raw
	08112014_102_JK_6-2014-BRO_SiHa1_fr18-20.raw	Raw
	08112014_103_JK_6-2014-BRO_SiHa1_fr20-22.raw	Raw
	08112014_104_JK_6-2014-BRO_SiHa1_fr22-24.raw	Raw

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Publications

Systems-level effects of ectopic galectin-7 reconstitution in cervical cancer and its microenvironment.

Higareda-Almaraz Juan Carlos JC Ruiz-Moreno Juan S JS Klimentova Jana J Barbieri Daniela D Salvador-Gallego Raquel R Ly Regina R Valtierra-Gutierrez Ilse A IA Dinsart Christiane C Rabinovich Gabriel A GA Stulik Jiri J Rösl Frank F Rincon-Orozco Bladimiro B

BMC cancer 20160824

<h4>Background</h4>Galectin-7 (Gal-7) is negatively regulated in cervical cancer, and appears to be a link between the apoptotic response triggered by cancer and the anti-tumoral activity of the immune system. Our understanding of how cervical cancer cells and their molecular networks adapt in response to the expression of Gal-7 remains limited.<h4>Methods</h4>Meta-analysis of Gal-7 expression was conducted in three cervical cancer cohort studies and TCGA. In silico prediction and bisulfite sequ ...[more]

PMID: 27558259

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Project description:Cervical cancer is still the leading cause of cancer mortality worldwide even after introduction of vaccine against Human papillomavirus (HPV), due to low vaccine coverage, especially in the developing world. Cervical cancer is primarily treated by Chemo/Radiotherapy, depending on the disease stage, with Carboplatin/Cisplatin-based drug regime. These drugs being non-specific, target rapidly dividing cells, including normal cells, so safer options are needed for lower off-target toxicity. Natural products offer an attractive option compared to synthetic drugs due to their well-established safety profile and capacity to target multiple oncogenic hallmarks of cancer like inflammation, angiogenesis, etc. In the current study, we investigated the effect of Bergenin (C-glycoside of 4-O-methylgallic acid), a natural polyphenol compound that is isolated from medicinal plants such as Bergenia crassifolia, Caesalpinia digyna, and Flueggea leucopyrus . Bergenin has been shown to have anti-inflammatory, anti-ulcerogenic, and wound healing properties but its anticancer potential has been realized only recently. We performed a proteomic analysis of cervical carcinoma cells treated with bergenin and found it to influence multiple hallmarks of cancers, including apoptosis, angiogenesis, and tumor suppressor proteins. It was also involved in many different cellular processes unrelated to cancer, as shown by our proteomic analysis. Further analysis showed bergenin to be a potent -angiogenic agent by reducing key angiogenic proteins like Galectin 3 and MMP-9 (Matrix Metalloprotease 9) in cervical carcinoma cells. Further understanding of this interaction was carried out using molecular docking analysis, which indicated MMP-9 has more affinity for bergenin as compared to Galectin-3. Cumulatively, our data provide novel insight into the anti-angiogenic mechanism of bergenin in cervical carcinoma cells by modulation of multiple angiogenic proteins like Galectin-3 and MMP-9 which warrant its further development as an anticancer agent in cervical cancer.

Project description:Identification of interactors is a major attempt in cell biology. Not only protein-protein but also protein-carbohydrate interactions are of high relevance for signal transduction in biological systems. Here we aim to identify novel interacting binding partners for the β-galactoside-binding proteins Galectin-1 (Gal-1) and Galectin-3 (Gal-3) in context of the eye disease proliferative vitreoretinopathy (PVR). PVR is one of the most common failures after retinal detachment surgeries and is characterized by the migration, adhesion and epithelial-to-mesenchymal transition (EMT) of retinal pigment epithelial cells (RPE) and the subsequent formation of sub- and epiretinal fibrocellular membranes. Gal-1 and Gal-3 bind in a dose- and carbohydrate-dependent manner to mesenchymal RPE cells and inhibit cellular processes like attachment and spreading. Yet knowledge about glycan-dependent interactors of Gal-1 and Gal-3 on RPE cells is very limited, although this is a prerequisite to unravel the influence of galectins on distinct cellular processes in RPE cells. In this approach, we identified by galectin pull-down experiments and quantitative proteomic screening 131 Galectin-3 and 15 Galectin-1 interactors. They mainly play a role in multiple binding processes and are mostly membrane proteins. Here we focused on two novel identified interactors of Gal-1 and Gal-3 in the context of PVR: the low-density lipoprotein receptor LRP1 and the platelet-derived growth factor receptor beta PDGFRB. We observed crosslinking and lattice formation of exogenous Gal-1 and Gal-3 with LRP1/PDGFRB and ITGB1 on the cell surface of human RPE cells. Weaker binding of Gal-1 and Gal-3 on these interactors and no lattice formation on the cell surface was seen, when complex-type-N-glycosylation was inhibited by treatment of the cells with Kifunensine. In conclusion, the identified specific glycoprotein ligands for Gal-1 and Gal-3 give us new insights in the highly specific binding of galectins to dedifferentiated RPE cells and the resulting prevention of PVR-associated cellular events.