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G protein subunit gamma 5 promotes the proliferation, metastasis and glycolysis of breast cancer cells through the Wnt/β-catenin pathway
GNG5 is suggested to exert a critical effect on tumor development in human beings; however, its function and related mechanism within breast cancer (BC) are still unclear. In this regard, the present work focused on identifying and evaluating GNG5’s function and revealing its possible molecular mech...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Lippincott Williams & Wilkins
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9575569/ https://www.ncbi.nlm.nih.gov/pubmed/36255067 http://dx.doi.org/10.1097/CAD.0000000000001394 |
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author | Yuan, Zuguo Ren, Ruiping Xu, Zhengyang |
author_facet | Yuan, Zuguo Ren, Ruiping Xu, Zhengyang |
author_sort | Yuan, Zuguo |
collection | PubMed |
description | GNG5 is suggested to exert a critical effect on tumor development in human beings; however, its function and related mechanism within breast cancer (BC) are still unclear. In this regard, the present work focused on identifying and evaluating GNG5’s function and revealing its possible molecular mechanism. Subcutaneous tumorigenesis model of nude mice and in-vitro cell model was established. The relationship between GNG5 expression and BC was studied through knockdown and overexpression experiments. The proliferation, migration, invasion and epithelial–mesenchymal transition (EMT) of liver cancer cell lines overexpressing or silencing GNG5 were detected. Furthermore, the pathway mechanism of GNG5 was evaluated at the molecular level and was performed to further verify the possible targets and mechanisms of action. In comparison with that in normal tissue, GNG5 level within BC tissue was higher. In addition, GNG5 overexpression stimulated BC cell proliferation, invasion, migration and EMT. BC cells with reduced GNG5 expression exhibited significant decreases in glucose uptake, lactate levels, and ATP concentrations. In addition, GNG5 knockdown inhibited Wnt/β-catenin signaling. This study indicates that GNG5 may generate a vital function in BC. The results of the current work demonstrated GNG5’s effect on BC pathological process, also providing a reference for developing new targeted therapies for BC. |
format | Online Article Text |
id | pubmed-9575569 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | Lippincott Williams & Wilkins |
record_format | MEDLINE/PubMed |
spelling | pubmed-95755692022-10-19 G protein subunit gamma 5 promotes the proliferation, metastasis and glycolysis of breast cancer cells through the Wnt/β-catenin pathway Yuan, Zuguo Ren, Ruiping Xu, Zhengyang Anticancer Drugs Original Studies GNG5 is suggested to exert a critical effect on tumor development in human beings; however, its function and related mechanism within breast cancer (BC) are still unclear. In this regard, the present work focused on identifying and evaluating GNG5’s function and revealing its possible molecular mechanism. Subcutaneous tumorigenesis model of nude mice and in-vitro cell model was established. The relationship between GNG5 expression and BC was studied through knockdown and overexpression experiments. The proliferation, migration, invasion and epithelial–mesenchymal transition (EMT) of liver cancer cell lines overexpressing or silencing GNG5 were detected. Furthermore, the pathway mechanism of GNG5 was evaluated at the molecular level and was performed to further verify the possible targets and mechanisms of action. In comparison with that in normal tissue, GNG5 level within BC tissue was higher. In addition, GNG5 overexpression stimulated BC cell proliferation, invasion, migration and EMT. BC cells with reduced GNG5 expression exhibited significant decreases in glucose uptake, lactate levels, and ATP concentrations. In addition, GNG5 knockdown inhibited Wnt/β-catenin signaling. This study indicates that GNG5 may generate a vital function in BC. The results of the current work demonstrated GNG5’s effect on BC pathological process, also providing a reference for developing new targeted therapies for BC. Lippincott Williams & Wilkins 2022-09-29 2022-11 /pmc/articles/PMC9575569/ /pubmed/36255067 http://dx.doi.org/10.1097/CAD.0000000000001394 Text en Copyright © 2022 The Author(s). Published by Wolters Kluwer Health, Inc. https://creativecommons.org/licenses/by-nc-nd/4.0/This is an open-access article distributed under the terms of the Creative Commons Attribution-Non Commercial-No Derivatives License 4.0 (CCBY-NC-ND) (https://creativecommons.org/licenses/by-nc-nd/4.0/) , where it is permissible to download and share the work provided it is properly cited. The work cannot be changed in any way or used commercially without permission from the journal. |
spellingShingle | Original Studies Yuan, Zuguo Ren, Ruiping Xu, Zhengyang G protein subunit gamma 5 promotes the proliferation, metastasis and glycolysis of breast cancer cells through the Wnt/β-catenin pathway |
title | G protein subunit gamma 5 promotes the proliferation, metastasis and glycolysis of breast cancer cells through the Wnt/β-catenin pathway |
title_full | G protein subunit gamma 5 promotes the proliferation, metastasis and glycolysis of breast cancer cells through the Wnt/β-catenin pathway |
title_fullStr | G protein subunit gamma 5 promotes the proliferation, metastasis and glycolysis of breast cancer cells through the Wnt/β-catenin pathway |
title_full_unstemmed | G protein subunit gamma 5 promotes the proliferation, metastasis and glycolysis of breast cancer cells through the Wnt/β-catenin pathway |
title_short | G protein subunit gamma 5 promotes the proliferation, metastasis and glycolysis of breast cancer cells through the Wnt/β-catenin pathway |
title_sort | g protein subunit gamma 5 promotes the proliferation, metastasis and glycolysis of breast cancer cells through the wnt/β-catenin pathway |
topic | Original Studies |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9575569/ https://www.ncbi.nlm.nih.gov/pubmed/36255067 http://dx.doi.org/10.1097/CAD.0000000000001394 |
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