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Galectins and galectin-mediated autophagy regulation: new insights into targeted cancer therapy
Galectins are animal lectins with specific affinity for galactosides via the conserved carbohydrate recognition domains. Increasing studies recently have identified critical roles of galectin family members in tumor progression. Abnormal expression of galectins contributes to the proliferation, meta...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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BioMed Central
2023
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9945697/ https://www.ncbi.nlm.nih.gov/pubmed/36814341 http://dx.doi.org/10.1186/s40364-023-00466-9 |
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author | Liu, Dan Zhu, Hongtao Li, Chuanzhou |
author_facet | Liu, Dan Zhu, Hongtao Li, Chuanzhou |
author_sort | Liu, Dan |
collection | PubMed |
description | Galectins are animal lectins with specific affinity for galactosides via the conserved carbohydrate recognition domains. Increasing studies recently have identified critical roles of galectin family members in tumor progression. Abnormal expression of galectins contributes to the proliferation, metastasis, epithelial-mesenchymal transformation (EMT), immunosuppression, radio-resistance and chemoresistance in various cancers, which has attracted cumulative clinical interest in galectin-based cancer treatment. Galectin family members have been reported to participate in autophagy regulation under physiological conditions and in non-tumoral diseases, and implication of galectins in multiple processes of carcinogenesis also involves regulation of autophagy, however, the relationship between galectins, autophagy and cancer remains largely unclear. In this review, we introduce the structure and function of galectins at the molecular level, summarize their engagements in autophagy and cancer progression, and also highlight the regulation of autophagy by galectins in cancer as well as the therapeutic potentials of galectin and autophagy-based strategies. Elaborating on the mechanism of galectin-regulated autophagy in cancers will accelerate the exploitation of galectins-autophagy targeted therapies in treatment for cancer. |
format | Online Article Text |
id | pubmed-9945697 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2023 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-99456972023-02-23 Galectins and galectin-mediated autophagy regulation: new insights into targeted cancer therapy Liu, Dan Zhu, Hongtao Li, Chuanzhou Biomark Res Review Galectins are animal lectins with specific affinity for galactosides via the conserved carbohydrate recognition domains. Increasing studies recently have identified critical roles of galectin family members in tumor progression. Abnormal expression of galectins contributes to the proliferation, metastasis, epithelial-mesenchymal transformation (EMT), immunosuppression, radio-resistance and chemoresistance in various cancers, which has attracted cumulative clinical interest in galectin-based cancer treatment. Galectin family members have been reported to participate in autophagy regulation under physiological conditions and in non-tumoral diseases, and implication of galectins in multiple processes of carcinogenesis also involves regulation of autophagy, however, the relationship between galectins, autophagy and cancer remains largely unclear. In this review, we introduce the structure and function of galectins at the molecular level, summarize their engagements in autophagy and cancer progression, and also highlight the regulation of autophagy by galectins in cancer as well as the therapeutic potentials of galectin and autophagy-based strategies. Elaborating on the mechanism of galectin-regulated autophagy in cancers will accelerate the exploitation of galectins-autophagy targeted therapies in treatment for cancer. BioMed Central 2023-02-22 /pmc/articles/PMC9945697/ /pubmed/36814341 http://dx.doi.org/10.1186/s40364-023-00466-9 Text en © The Author(s) 2023 https://creativecommons.org/licenses/by/4.0/Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) . The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/ (https://creativecommons.org/publicdomain/zero/1.0/) ) applies to the data made available in this article, unless otherwise stated in a credit line to the data. |
spellingShingle | Review Liu, Dan Zhu, Hongtao Li, Chuanzhou Galectins and galectin-mediated autophagy regulation: new insights into targeted cancer therapy |
title | Galectins and galectin-mediated autophagy regulation: new insights into targeted cancer therapy |
title_full | Galectins and galectin-mediated autophagy regulation: new insights into targeted cancer therapy |
title_fullStr | Galectins and galectin-mediated autophagy regulation: new insights into targeted cancer therapy |
title_full_unstemmed | Galectins and galectin-mediated autophagy regulation: new insights into targeted cancer therapy |
title_short | Galectins and galectin-mediated autophagy regulation: new insights into targeted cancer therapy |
title_sort | galectins and galectin-mediated autophagy regulation: new insights into targeted cancer therapy |
topic | Review |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9945697/ https://www.ncbi.nlm.nih.gov/pubmed/36814341 http://dx.doi.org/10.1186/s40364-023-00466-9 |
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