The role of glycans in the mechanobiology of cancer

Purushothaman, Anurag; Mohajeri, M. Hasan; Lele, Tanmay P.

doi:10.1016/j.jbc.2023.102935

Cited by 14 publications

(3 citation statements)

References 220 publications

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“…GAGs are linear polyanionic animal heteropolysaccharides, which can be classified into four groups according to the structure of disaccharide units: heparin/heparin sulfate, chondroitin/chondroitin sulfate, keratin sulfate, and HA ( Song Y. et al, 2021 ). PGs are a class of modified proteins formed by the covalent binding of GAGs (such as chondroitin sulfate or heparin sulfate chains) other than HA to the protein core ( Wang and Chi, 2022 ; Purushothaman et al, 2023 ). PGs have been shown to enhance the remodeling capacity of liver tissue, and their numbers are significantly increased in cirrhotic liver tumors, especially perlecan and decorin, and the knockout of perlecan and decorin also leads to a decrease in ECM stiffness ( Kovalszky et al, 1993 ; Kimura et al, 2008 ; Robinson et al, 2017 ).…”

Section: Extracellular Matrix Remodeling In Hepatic Fibrosismentioning

confidence: 99%

“…Elastin is present in the walls of blood vessels, the capsule, and long-term fibrotic tissues, and can provide reversible elasticity to the organ to relieve mechanical loading ( Cocciolone et al, 2018 ). GAGs are fibrous, rigid, unbranched polysaccharide chains that are composed of repeating disaccharide units, present as free sugar chains [e.g., hyaluronic acid (HA) ], or attached primarily to PGs (e.g., heparan sulfate or chondroitin sulfate chains) ( Purushothaman et al, 2023 ). PGs are hydrated gels with a certain consistency that regulate cell adhesion and maintain hyperosmolality ( Khurana et al, 2021 ).…”

Section: Introduction To the Extracellular Matrixmentioning

confidence: 99%

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Mechanical homeostasis imbalance in hepatic stellate cells activation and hepatic fibrosis

Zhao

Deng

et al. 2023

Front. Mol. Biosci.

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Chronic liver disease or repeated damage to hepatocytes can give rise to hepatic fibrosis. Hepatic fibrosis (HF) is a pathological process of excessive sedimentation of extracellular matrix (ECM) proteins such as collagens, glycoproteins, and proteoglycans (PGs) in the hepatic parenchyma. Changes in the composition of the ECM lead to the stiffness of the matrix that destroys its inherent mechanical homeostasis, and a mechanical homeostasis imbalance activates hepatic stellate cells (HSCs) into myofibroblasts, which can overproliferate and secrete large amounts of ECM proteins. Excessive ECM proteins are gradually deposited in the Disse gap, and matrix regeneration fails, which further leads to changes in ECM components and an increase in stiffness, forming a vicious cycle. These processes promote the occurrence and development of hepatic fibrosis. In this review, the dynamic process of ECM remodeling of HF and the activation of HSCs into mechanotransduction signaling pathways for myofibroblasts to participate in HF are discussed. These mechanotransduction signaling pathways may have potential therapeutic targets for repairing or reversing fibrosis.

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Section: Extracellular Matrix Remodeling In Hepatic Fibrosismentioning

confidence: 99%

Section: Introduction To the Extracellular Matrixmentioning

confidence: 99%

Mechanical homeostasis imbalance in hepatic stellate cells activation and hepatic fibrosis

Zhao

Deng

et al. 2023

Front. Mol. Biosci.

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“…In turn, the intra-and extracellular K + concentrations are one of the regulating factors for glycolysis and OxPhos [13,27]. Considering the altered glycome in can-cer, it affects-globally-the biophysical properties of membranes [28] (thus, it indirectly influences the potassium channels' activity via protein-lipid and protein-protein interactions [29,30]) and-locally-the glycosylation of the structure of the channels, which predefines their functionality [31][32][33][34][35]. In this work, we focus on the second aspect, which more evidently affects the channel activity.…”

Section: Introductionmentioning

confidence: 99%

Potassium Channels, Glucose Metabolism and Glycosylation in Cancer Cells

Wawrzkiewicz-Jałowiecka

Lalik

Łukasiak

et al. 2023

IJMS

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Potassium channels emerge as one of the crucial groups of proteins that shape the biology of cancer cells. Their involvement in processes like cell growth, migration, or electric signaling, seems obvious. However, the relationship between the function of K+ channels, glucose metabolism, and cancer glycome appears much more intriguing. Among the typical hallmarks of cancer, one can mention the switch to aerobic glycolysis as the most favorable mechanism for glucose metabolism and glycome alterations. This review outlines the interconnections between the expression and activity of potassium channels, carbohydrate metabolism, and altered glycosylation in cancer cells, which have not been broadly discussed in the literature hitherto. Moreover, we propose the potential mediators for the described relations (e.g., enzymes, microRNAs) and the novel promising directions (e.g., glycans-orinented drugs) for further research.

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Metabolic‐Glycoengineering‐Enabled Molecularly Specific Acoustic Tweezing Cytometry for Targeted Mechanical Stimulation of Cell Surface Sialoglycans

Li,

Guo,

Hobson

et al. 2024

Angewandte Chemie

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This study developed a new type of dibenzocyclooctyne (DBCO)‐functionalized microbubbles (MBs) and validated their attachment to azide‐labelled sialoglycans on human pluripotent stem cells (hPSCs) generated via metabolic glycoengineering (MGE). This enabled application of mechanical forces to sialoglycans on hPSCs via molecularly specific acoustic tweezing cytometry (mATC), i.e., displacing sialoglycan‐anchored MBs using ultrasound (US). It was shown that subjected to forces of US pulses, sialoglycan‐anchored MBs exhibited significantly larger displacements and faster, more complete recovery after each pulse than integrin‐anchored MBs, indicating that sialoglycans are more stretchable and elastic than integrins on hPSCs in response to mechanical force. Furthermore, stimulating sialoglycans on hPSCs using mATC reduced stage‐specific embryonic antigen‐3 (SSEA‐3) and GD3 expression but not OCT4 and SOX2 nuclear localization. Conversely, stimulating integrins decreased OCT4 nuclear localization but not SSEA‐3 and GD3 expression, suggesting that mechanically stimulating sialoglycans and integrins initiated distinct mechanoresponses during the early stages of hPSC differentiation. Taken together, the results demonstrated that MGE‐enabled mATC uncovered not only different mechanical properties of sialoglycans on hPSCs than integrins but also their different mechanoregulatory impacts on hPSC differentiation, validating MGE‐based mATC as a new, powerful tool for investigating the roles of glycans and other cell surface biomolecules in mechanotransduction.

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The role of glycans in the mechanobiology of cancer

Cited by 14 publications

References 220 publications

Mechanical homeostasis imbalance in hepatic stellate cells activation and hepatic fibrosis

Mechanical homeostasis imbalance in hepatic stellate cells activation and hepatic fibrosis

Potassium Channels, Glucose Metabolism and Glycosylation in Cancer Cells

Metabolic‐Glycoengineering‐Enabled Molecularly Specific Acoustic Tweezing Cytometry for Targeted Mechanical Stimulation of Cell Surface Sialoglycans

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