Expression of galectin-1 and galectin-3 in renal cell carcinoma; immunohistochemical study

Aboulhagag, Noha A.; El-Deek, Heba E M; Sherif, M. K.

doi:10.1016/j.anndiagpath.2018.06.005

Cited by 10 publications

(4 citation statements)

References 27 publications

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“…Increasing evidence has shown that TCN1 is highly expressed in metastatic epithelial tumors such as breast cancer, thyroid cancer, laryngeal cancer, and cervical cancer [9,11,12,14,40,41]. Bioinformatics analysis and meta-data analysis based on the COAD database showed that TCN1 was overexpressed as an oncogene in colorectal cancer [15].…”

Section: Discussionmentioning

confidence: 99%

TCN1 Deficiency Inhibits The Malignancy of Colorectal Cancer Cells By Regulating The ITGB4 Pathway

Zhu

Jiang

Huang

et al. 2021

Preprint

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Background: This study aimed to investigate the biological function and regulatory mechanism of TCN1 in colorectal cancer (CRC). Methods: We studied the biological functions of TCN1 using gain-of-function and loss-of-function analysis in HCT116 cell lines, and examined the effects of TCN1 on the proliferation, apoptosis, and invasion of CRC cells and determined its potential molecular mechanisms using CRC lines and mouse xenotransplantation models. Tumor xenograft and tumor metastasis studies were performed to detect the tumorigenicity and metastasis of cells in vivo. Results: TCN1-knockdown attenuated CRC cell proliferation, invasion and promoted cell apoptosis. Overexpression of TCN1 yielded the opposite effects. In addition, TCN1-knockdown HCT116 cells failed to form metastatic foci in the peritoneum after intravenous injection. Molecular mechanism studies showed that TCN1 interacts with integrin subunit β4 (ITGB4) to positively regulate the expression of ITGB4. TCN1-knockdown promoted the degradation of ITGB4 and increased the instability of ITGB4 and filamin A (FLNA). Downregulation of ITGB4 at the protein level resulted in the disassociation of the ITGB4/PLEC complex, leading to cytoskeletal damage. Conclusion: TCN1 might exert oncogenic role in CRC via regulating the ITGB4 signaling pathway.

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Section: Discussionmentioning

confidence: 99%

TCN1 Deficiency Inhibits The Malignancy of Colorectal Cancer Cells By Regulating The ITGB4 Pathway

Zhu

Jiang

Huang

et al. 2021

Preprint

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“…Accordingly, Gal7 sensitized tumor cells to cisplatin treatment by promoting the accumulation of intracellular reactive oxygen species and activation of the JNK pathway ( Matsui et al, 2007 ). Finally, recent studies showed an inverse correlation between Gal3 expression and the extent of tumor necrosis in renal cell carcinoma patients ( Aboulhagag et al, 2018 ). Thus, intracellular galectins may govern cell death pathways, including apoptosis, necrosis, or autophagy, induced by pro-inflammatory cytokines, reactive oxygen species, and anticancer agents.…”

Section: Developing Resistance To Cell Deathmentioning

confidence: 96%

“…recent studies showed an inverse correlation between Gal3 expression and the extent of tumor necrosis in renal cell carcinoma patients (Aboulhagag et al, 2018). Thus, intracellular galectins may govern cell death pathways, including apoptosis, necrosis, or autophagy, induced by pro-inflammatory cytokines, reactive oxygen species, and anticancer agents.…”

Section: Acquiring Genome Instabilitymentioning

confidence: 98%

Sweetening the hallmarks of cancer: Galectins as multifunctional mediators of tumor progression

Girotti

Salatino

Dalotto-Moreno

et al. 2019

Journal of Experimental Medicine

136

123

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Hanahan and Weinberg have proposed 10 organizing principles that enable growth and metastatic dissemination of cancer cells. These distinctive and complementary capabilities, defined as the “hallmarks of cancer,” include the ability of tumor cells and their microenvironment to sustain proliferative signaling, evade growth suppressors, resist cell death, promote replicative immortality, induce angiogenesis, support invasion and metastasis, reprogram energy metabolism, induce genomic instability and inflammation, and trigger evasion of immune responses. These common features are hierarchically regulated through different mechanisms, including those involving glycosylation-dependent programs that influence the biological and clinical impact of each hallmark. Galectins, an evolutionarily conserved family of glycan-binding proteins, have broad influence in tumor progression by rewiring intracellular and extracellular circuits either in cancer or stromal cells, including immune cells, endothelial cells, and fibroblasts. In this review, we dissect the role of galectins in shaping cellular circuitries governing each hallmark of tumors, illustrating relevant examples and highlighting novel opportunities for treating human cancer.

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“…endothelial cells, macrophages and etc. Galectin-3 mediates various biological functions, such as cells attachment, differentiation and proliferation, in ammatory in ltration, cancer invasion and angiogenesis [8,9] . AGEs are formed by their aldehyde functionalgroup of the sugar with an amine or guanidine group of theamino acid via non-enzymatic glycation reactions, the increased accumulation of AGEs direct cause severe metabolic disorders.…”

Section: Introductionmentioning

confidence: 99%

Catalpol prevents glomerular angiogenesis induced by advanced glycation end products via inhibiting Galectin-3

Sun

Gao

Cao

et al. 2022

Preprint

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Objectives: The main characteristics of Diabetic Nephropathy (DN) at the early stage is abnormal angiogenesis of glomerular endothelial cells and macrophage infiltration. Galectin-3 plays a pivotal role in the pathogenesis of DN via binding with its ligand, Advanced Glycation End products (AGEs). Catalpol (Cat.), an iridoid glucoside extracted fromRehmannia glutinosa, has been found to ameliorate vascular inflammation, reduce endothelial permeability and protect endothelial damage upon diabetic milieu. However, little is known about whether Cat. could exert anti-angiogenesis and anti-inflammation effect induced by AGEs. Methods:The anti-angiogenic mechanisms of Cat. were examined by incubating mouse glomerular endothelial cells (mGECs) and RAW 264.7 macrophages induced by AGEs. The expression of Galectin-3 and correlated molecules were also detected in diabetic rats treated with Cat.Key findings: We observed that Galectin-3/Hypoxia-inducible factor-1(HIF-1α)was activated by AGEs in mGECs and RAW 264.7 macrophages, catalpol significantly inhibited the proliferation of the mGECs and RAW 264.7 macrophages in vitro.Meanwhile, it also ameliorateddiabetes-induced renal damage via inhibiting Galectin-3/VEGF/HIF-1α pathways in vivo.Conclusions: Altogether, our findings demonstrated that Cat. prevent the angiogenesis of mGECs and macrophages proliferation via inhibiting Galectin-3. We suggest that Cat.contributes to block the pathogenic development of diabetes-induced renal damage.

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Expression of galectin-1 and galectin-3 in renal cell carcinoma; immunohistochemical study

Cited by 10 publications

References 27 publications

TCN1 Deficiency Inhibits The Malignancy of Colorectal Cancer Cells By Regulating The ITGB4 Pathway

TCN1 Deficiency Inhibits The Malignancy of Colorectal Cancer Cells By Regulating The ITGB4 Pathway

Sweetening the hallmarks of cancer: Galectins as multifunctional mediators of tumor progression

Catalpol prevents glomerular angiogenesis induced by advanced glycation end products via inhibiting Galectin-3

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