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Hsa_circ_0001944 enhanced GSPT1 expression via sponging miR‐498 to promote proliferation and invasion of gastric cancer
BACKGROUND: Gastric cancer (GC) is the fifth most common malignant tumor and the third leading cause of cancer‐related deaths worldwide. CircRNAs may provide new insights into the development of GC by acting as oncogenes or tumor suppressors. In this study, we aim to examine the biological role of h...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
John Wiley and Sons Inc.
2023
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9937881/ https://www.ncbi.nlm.nih.gov/pubmed/36597856 http://dx.doi.org/10.1002/jcla.24810 |
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author | Liu, Rujiao Han, Xiaotian Gao, Shuiping Chen, Yang Zhang, Jian |
author_facet | Liu, Rujiao Han, Xiaotian Gao, Shuiping Chen, Yang Zhang, Jian |
author_sort | Liu, Rujiao |
collection | PubMed |
description | BACKGROUND: Gastric cancer (GC) is the fifth most common malignant tumor and the third leading cause of cancer‐related deaths worldwide. CircRNAs may provide new insights into the development of GC by acting as oncogenes or tumor suppressors. In this study, we aim to examine the biological role of hsa_circ_0001944 (circFIRRE) in tumor progression of GC. METHODS: The bioinformatic analysis, qPCR, Western blotting, and immunohistochemistry were fulfilled to detect the expression of hsa_circ_0001944, miR‐498, and GSPT1 in gastric cancer. Gain or loss of function approaches were used to investigate the biological functions of hsa_circ_0001944. MTS, EDU, wound healing, and transwell assays were performed to study the proliferation, invasion, and migration of GC cells. These molecular mechanisms were detected by luciferase reporter assays and chromatin immunoprecipitation assays. RESULTS: We screened out hsa_circ_0001944, whose expression was significantly increased in gastric cancer tissues. Knockdown of hsa_circ_0001944 significantly suppressed the cell proliferation, invasion, and migration. Mechanistic investigations showed that hsa_circ_0001944 can bind to and sponge miR‐498. Moreover, hsa_circ_0001944 sponged miR‐498 to increase GSPT1 expression, thereby promoted excessive proliferation and maintained the malignant phenotype of GC cells. CONCLUSION: The present study demonstrates the hsa_circ_0001944/miR‐498/GSPT1 axis contributes to GC development. This may provide a target for GC therapy and potential prognostic biomarker. |
format | Online Article Text |
id | pubmed-9937881 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2023 |
publisher | John Wiley and Sons Inc. |
record_format | MEDLINE/PubMed |
spelling | pubmed-99378812023-02-19 Hsa_circ_0001944 enhanced GSPT1 expression via sponging miR‐498 to promote proliferation and invasion of gastric cancer Liu, Rujiao Han, Xiaotian Gao, Shuiping Chen, Yang Zhang, Jian J Clin Lab Anal Research Articles BACKGROUND: Gastric cancer (GC) is the fifth most common malignant tumor and the third leading cause of cancer‐related deaths worldwide. CircRNAs may provide new insights into the development of GC by acting as oncogenes or tumor suppressors. In this study, we aim to examine the biological role of hsa_circ_0001944 (circFIRRE) in tumor progression of GC. METHODS: The bioinformatic analysis, qPCR, Western blotting, and immunohistochemistry were fulfilled to detect the expression of hsa_circ_0001944, miR‐498, and GSPT1 in gastric cancer. Gain or loss of function approaches were used to investigate the biological functions of hsa_circ_0001944. MTS, EDU, wound healing, and transwell assays were performed to study the proliferation, invasion, and migration of GC cells. These molecular mechanisms were detected by luciferase reporter assays and chromatin immunoprecipitation assays. RESULTS: We screened out hsa_circ_0001944, whose expression was significantly increased in gastric cancer tissues. Knockdown of hsa_circ_0001944 significantly suppressed the cell proliferation, invasion, and migration. Mechanistic investigations showed that hsa_circ_0001944 can bind to and sponge miR‐498. Moreover, hsa_circ_0001944 sponged miR‐498 to increase GSPT1 expression, thereby promoted excessive proliferation and maintained the malignant phenotype of GC cells. CONCLUSION: The present study demonstrates the hsa_circ_0001944/miR‐498/GSPT1 axis contributes to GC development. This may provide a target for GC therapy and potential prognostic biomarker. John Wiley and Sons Inc. 2023-01-04 /pmc/articles/PMC9937881/ /pubmed/36597856 http://dx.doi.org/10.1002/jcla.24810 Text en © 2023 The Authors. Journal of Clinical Laboratory Analysis published by Wiley Periodicals LLC. https://creativecommons.org/licenses/by/4.0/This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Research Articles Liu, Rujiao Han, Xiaotian Gao, Shuiping Chen, Yang Zhang, Jian Hsa_circ_0001944 enhanced GSPT1 expression via sponging miR‐498 to promote proliferation and invasion of gastric cancer |
title | Hsa_circ_0001944 enhanced GSPT1 expression via sponging miR‐498 to promote proliferation and invasion of gastric cancer |
title_full | Hsa_circ_0001944 enhanced GSPT1 expression via sponging miR‐498 to promote proliferation and invasion of gastric cancer |
title_fullStr | Hsa_circ_0001944 enhanced GSPT1 expression via sponging miR‐498 to promote proliferation and invasion of gastric cancer |
title_full_unstemmed | Hsa_circ_0001944 enhanced GSPT1 expression via sponging miR‐498 to promote proliferation and invasion of gastric cancer |
title_short | Hsa_circ_0001944 enhanced GSPT1 expression via sponging miR‐498 to promote proliferation and invasion of gastric cancer |
title_sort | hsa_circ_0001944 enhanced gspt1 expression via sponging mir‐498 to promote proliferation and invasion of gastric cancer |
topic | Research Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9937881/ https://www.ncbi.nlm.nih.gov/pubmed/36597856 http://dx.doi.org/10.1002/jcla.24810 |
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