Glycobiology of cell death: when glycans and lectins govern cell fate

Lichtenstein, Rachel G.; Rabinovich, Gabriel A.

doi:10.1038/cdd.2013.50

Cited by 89 publications

(59 citation statements)

References 120 publications

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“…This protein can be expressed and affect chemoresistance, resulting from induction by several signaling pathways required for CSC survival, such as IL-4 [46], Akt/PKB signaling [47], or Aurora-A [48]. Galectin-3 has been demonstrated to form heterodimers with Bcl-2, or may directly interact with the mitochondrial permeability transition pore complex and regulate its opening, preventing the release of cytochrome c [49, 50]. Moreover, galectin-3 can also inhibit cisplatin-induced poly(ADP-ribose) polymerase degradation and apoptosis, without alter Bcl-2, Bcl-XL, or Bax expressions [29].…”

Section: Discussionmentioning

confidence: 99%

Galectin-3 augments tumor initiating property and tumorigenicity of lung cancer through interaction with β-catenin

Chung

Tang

et al. 2014

Oncotarget

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Cancer stem cells (CSCs) are comprised of a rare sub-population of cells in tumors that have been proposed to be responsible for high recurrence rates and resistance to chemotherapy. Galectins are highly expressed in cancers that correlate with the aggressiveness of tumors. Galectins may also promote the resistance of cancer cells to chemotherapy. However, the role of galectins in CSCs remains unknown. In this study, sphere formation was used to enrich H1299 human lung CSCs that had self-renewal ability, advanced tumorigenic potential, and that highly expressed stem/progenitor cell markers such as Oct4, Sox2, Nanog, and CD133. A novel candidate molecule, galectin-3, for stemness was found in lung CSCs. The expression of galectin-3 robustly increased in lung cancer spheres over serial passages, but its suppression in the H1299 monolayer or spheres resulted in reduced expression of stemness-related genes, sphere-forming ability, tumorigenicity, chemoresistance, and tumor initiation in mice. Notably, the overexpression of galectin-3 in A549 lung cancer cells, which have low capability to grow as tumor spheres, promoted CSC formation. β-catenin activity was increased in H1299 spheres and counteracted by galectin-3 suppression. Thus, galectin-3 may act as a cofactor by interacting with β-catenin to augment the transcriptional activities of stemness-related genes. Furthermore, galectin-3 expression correlated with tumor progression and expressions of β-catenin and CSC marker CD133 in lung cancer tissues. Targeting galectin-3 signaling may provide a new strategy for lung cancer treatment by inhibiting stem-like properties.

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Section: Discussionmentioning

confidence: 99%

Galectin-3 augments tumor initiating property and tumorigenicity of lung cancer through interaction with β-catenin

Chung

Tang

et al. 2014

Oncotarget

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“…Tumorigenic cells possess the change of glycosylation modification, which may lead to metastasis, uncontrolled proliferation, and the inhibition of apoptosis. [14][15][16] It has been reported that protein glycosylation was involved in potentially all aspects of human growth and development. Altered glycans on the tumor-and host-cell surface and in the tumor microenvironment have been identified to mediate critical events at the onset and/or during tumor progression.…”

Section: Introductionmentioning

confidence: 99%

The role of epithelial cell adhesion molecule N-glycosylation on apoptosis in breast cancer cells

Zhang

Gao

et al. 2017

Tumour Biol.

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Glycosylation of cell surface proteins plays an important role in the regulation of apoptosis. It has been demonstrated that knockdown of epithelial cell adhesion molecule promoted apoptosis, inhibited cell proliferation, and caused cell-cycle arrest. In this study, we investigated whether and how N-glycosylation of epithelial cell adhesion molecule influenced the apoptosis in breast cancer cells. We applied the N-glycosylation mutation epithelial cell adhesion molecule plasmid to express deglycosylation of epithelial cell adhesion molecule and then to study its function. Our results showed that deglycosylation of epithelial cell adhesion molecule promoted apoptosis and inhibited cell proliferation. Deglycosylation of epithelial cell adhesion molecule enhanced the cytotoxic effect of 5-fluorouracil, promoting apoptosis by downregulating the expression of the anti-apoptotic protein Bcl-2 and upregulating the expression of the pro-apoptotic proteins Bax and Caspase 3 via the extracellular-signal-regulated kinase 1/2 and c-Jun N-terminal kinase mitogen-activated protein kinase signaling pathways in MCF-7 and MDA-MB-231 cells. These findings are important for a better understanding of epithelial cell adhesion molecule apoptosis regulation and suggest epithelial cell adhesion molecule as a potential target for the treatment of breast cancer.

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“…42 We can also speculate that N-acetylglucosaminyltransferase GCNT3 contributes to the glycosylation of TRAIL receptors, which is critical for their function. 43,44 In addition, substance P stimulates p21-activated kinase, 45 which is a known regulator of the mitogen-activated protein kinases (MAPK) cascade. 46 In turn, MAPKs, at least in some cases, may sensitize cells to TRAIL-induced apoptosis.…”

Section: Discussionmentioning

confidence: 99%

An RNA interference screen identifies new avenues for nephroprotection

et al. 2015

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Acute kidney injury is a major public health problem, which is commonly caused by renal ischemia and is associated with a high risk of mortality and long-term disability. Efforts to develop a treatment for this condition have met with very limited success. We used an RNA interference screen to identify genes (BCL2L14, BLOC1S2, C2ORF42, CPT1A, FBP1, GCNT3, RHOB, SCIN, TACR1, and TNFAIP6) whose suppression improves survival of kidney epithelial cells in in vitro models of oxygen and glucose deprivation. Some of the genes also modulate the toxicity of cisplatin, an anticancer agent whose use is currently limited by nephrotoxicity. Furthermore, pharmacological inhibition of TACR1 product NK1R was protective in a model of mouse renal ischemia, attesting to the in vivo relevance of our findings. These data shed new light on the mechanisms of stress response in mammalian cells, and open new avenues to reduce the morbidity and mortality associated with renal injury.

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Glycobiology of cell death: when glycans and lectins govern cell fate

Cited by 89 publications

References 120 publications

Galectin-3 augments tumor initiating property and tumorigenicity of lung cancer through interaction with β-catenin

Galectin-3 augments tumor initiating property and tumorigenicity of lung cancer through interaction with β-catenin

The role of epithelial cell adhesion molecule N-glycosylation on apoptosis in breast cancer cells

An RNA interference screen identifies new avenues for nephroprotection

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