Hypoxia promotes metastasis by relieving miR-598-3p-restricted glycolysis in gastric cancer
Abstract The activation of glycolysis, particularly in the context of reprogrammed energy metabolism, is increasingly recognized as a significant characteristic of cancer. However, the precise mechanisms by which glycolysis is promoted in metastatic gastric cancer cells under normal oxygen condition...
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BMC
2024-03-01
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Series: | Journal of Translational Medicine |
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Online Access: | https://doi.org/10.1186/s12967-024-04957-7 |
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author | Wei Zhou Mengyuan Tang Dan He Yi Shen Ziwei Huang Wenxin Xia Zhiyun Wu Wenxiang Wei Hui Zheng Qi Wang Weifeng Shi Jingting Jiang |
author_facet | Wei Zhou Mengyuan Tang Dan He Yi Shen Ziwei Huang Wenxin Xia Zhiyun Wu Wenxiang Wei Hui Zheng Qi Wang Weifeng Shi Jingting Jiang |
author_sort | Wei Zhou |
collection | DOAJ |
description | Abstract The activation of glycolysis, particularly in the context of reprogrammed energy metabolism, is increasingly recognized as a significant characteristic of cancer. However, the precise mechanisms by which glycolysis is promoted in metastatic gastric cancer cells under normal oxygen conditions remain poorly understood. MicroRNAs (miRNAs) play a crucial role in the development of malignant phenotypes in gastric cancer. Nevertheless, our understanding of the specific involvement of miRNAs in hypoxia-induced metabolic shifting and the subsequent metastatic processes is limited. Hypoxia-induced downregulation of miR-598-3p mechanistically leads to the upregulation of RMP and IGF1r, thereby promoting glycolysis. Either overexpression of miR-598-3p or R406 treatment effectively suppresses the metastasis of gastric cancer cells both in vitro and in vivo. Collectively, the depletion of miR-598-3p alters glucose metabolism from oxidative phosphorylation to glycolysis, thereby exacerbating the malignancy of gastric cancer cells. The present findings indicate a potential target for the development of therapeutics against gastric cancers with increased miR-598-3p expression. |
first_indexed | 2024-04-24T23:03:50Z |
format | Article |
id | doaj.art-8ed18ededead46eaadd7d1ab8d1817d6 |
institution | Directory Open Access Journal |
issn | 1479-5876 |
language | English |
last_indexed | 2024-04-24T23:03:50Z |
publishDate | 2024-03-01 |
publisher | BMC |
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series | Journal of Translational Medicine |
spelling | doaj.art-8ed18ededead46eaadd7d1ab8d1817d62024-03-17T12:36:43ZengBMCJournal of Translational Medicine1479-58762024-03-0122111610.1186/s12967-024-04957-7Hypoxia promotes metastasis by relieving miR-598-3p-restricted glycolysis in gastric cancerWei Zhou0Mengyuan Tang1Dan He2Yi Shen3Ziwei Huang4Wenxin Xia5Zhiyun Wu6Wenxiang Wei7Hui Zheng8Qi Wang9Weifeng Shi10Jingting Jiang11Department of Clinical Laboratory, The Third Affiliated Hospital of Soochow UniversityDepartment of Clinical Laboratory, The Third Affiliated Hospital of Soochow UniversityDepartment of Clinical Laboratory, The Third Affiliated Hospital of Soochow UniversityDepartment of Clinical Laboratory, The Third Affiliated Hospital of Soochow UniversityDepartment of Clinical Laboratory, The Third Affiliated Hospital of Soochow UniversityDepartment of Clinical Laboratory, The Third Affiliated Hospital of Soochow UniversityDepartment of Clinical Laboratory, The Third Affiliated Hospital of Soochow UniversityDepartment of Cell Biology, Soochow UniversityDepartment of Clinical Laboratory, The Third Affiliated Hospital of Soochow UniversityDepartment of Biological Treatment, The Third Affiliated Hospital of Soochow UniversityDepartment of Clinical Laboratory, The Third Affiliated Hospital of Soochow UniversityDepartment of Biological Treatment, The Third Affiliated Hospital of Soochow UniversityAbstract The activation of glycolysis, particularly in the context of reprogrammed energy metabolism, is increasingly recognized as a significant characteristic of cancer. However, the precise mechanisms by which glycolysis is promoted in metastatic gastric cancer cells under normal oxygen conditions remain poorly understood. MicroRNAs (miRNAs) play a crucial role in the development of malignant phenotypes in gastric cancer. Nevertheless, our understanding of the specific involvement of miRNAs in hypoxia-induced metabolic shifting and the subsequent metastatic processes is limited. Hypoxia-induced downregulation of miR-598-3p mechanistically leads to the upregulation of RMP and IGF1r, thereby promoting glycolysis. Either overexpression of miR-598-3p or R406 treatment effectively suppresses the metastasis of gastric cancer cells both in vitro and in vivo. Collectively, the depletion of miR-598-3p alters glucose metabolism from oxidative phosphorylation to glycolysis, thereby exacerbating the malignancy of gastric cancer cells. The present findings indicate a potential target for the development of therapeutics against gastric cancers with increased miR-598-3p expression.https://doi.org/10.1186/s12967-024-04957-7Glucose metabolismMetastasisHypoxiamicroRNAsGastric cancer |
spellingShingle | Wei Zhou Mengyuan Tang Dan He Yi Shen Ziwei Huang Wenxin Xia Zhiyun Wu Wenxiang Wei Hui Zheng Qi Wang Weifeng Shi Jingting Jiang Hypoxia promotes metastasis by relieving miR-598-3p-restricted glycolysis in gastric cancer Journal of Translational Medicine Glucose metabolism Metastasis Hypoxia microRNAs Gastric cancer |
title | Hypoxia promotes metastasis by relieving miR-598-3p-restricted glycolysis in gastric cancer |
title_full | Hypoxia promotes metastasis by relieving miR-598-3p-restricted glycolysis in gastric cancer |
title_fullStr | Hypoxia promotes metastasis by relieving miR-598-3p-restricted glycolysis in gastric cancer |
title_full_unstemmed | Hypoxia promotes metastasis by relieving miR-598-3p-restricted glycolysis in gastric cancer |
title_short | Hypoxia promotes metastasis by relieving miR-598-3p-restricted glycolysis in gastric cancer |
title_sort | hypoxia promotes metastasis by relieving mir 598 3p restricted glycolysis in gastric cancer |
topic | Glucose metabolism Metastasis Hypoxia microRNAs Gastric cancer |
url | https://doi.org/10.1186/s12967-024-04957-7 |
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