MicroRNA-32-5p promotes the proliferation and metastasis of gastric cancer cells

Abstract Gastric cancer (GC) is a huge threat to global health, there is no effective treatment or just delay the progression of advanced GC until now. Micro-RNAs were reported to participate in the progression of GC. Clonal formation, MTT, caspase-3 activity, sperm DNA fragmentation, flow cytometry...

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Main Authors: Chao Sun, Lai-gang Huang, Bing Leng, Yanting Guo, Chen Chen, Ruijie Lv, Yan Dong, Tian-tian Gao, De-qing Sun
Format: Article
Language:English
Published: Nature Portfolio 2025-01-01
Series:Scientific Reports
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Online Access:https://doi.org/10.1038/s41598-025-86367-3
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author Chao Sun
Lai-gang Huang
Bing Leng
Yanting Guo
Chen Chen
Ruijie Lv
Yan Dong
Tian-tian Gao
De-qing Sun
author_facet Chao Sun
Lai-gang Huang
Bing Leng
Yanting Guo
Chen Chen
Ruijie Lv
Yan Dong
Tian-tian Gao
De-qing Sun
author_sort Chao Sun
collection DOAJ
description Abstract Gastric cancer (GC) is a huge threat to global health, there is no effective treatment or just delay the progression of advanced GC until now. Micro-RNAs were reported to participate in the progression of GC. Clonal formation, MTT, caspase-3 activity, sperm DNA fragmentation, flow cytometry assay, cell adhesion, transwell assays were performed to detect the functions of miR-32-5p or anti-miR-32-5p on the growth and metastasis of GC cells. Western blot, qRT-PCR, Co-immunoprecipitation, and luciferase reporter analysis were performed to explore the associated mechanisms. We established mouse tumor xenografts and mouse metastasis models to explore the role of miR-32-5p and anti-miR-32-5p in vivo. We found that miR-32-5p significantly promoting the proliferation and metastasis of GC cells at both in vitro and in vivo levels. The underlying mechanism maybe that miR-32-5p complementary paired with the 3′-UTR of DSC2, and inhibited the expression of DSC2. Furthermore, we found that DSC2 suppressed the transcription of Cyclin B1, and induced G2/M phase arrest through inhibiting the complex of β-catenin/TCF4 in nucleus. We concluded that miR-32-5p negatively regulated the DSC2 expression, might be a potential therapeutic targeting of cancers, most especially in GC.
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spelling doaj-art-977d38c9211e4d8195ee72feb2e91dc22025-01-26T12:28:24ZengNature PortfolioScientific Reports2045-23222025-01-0115111410.1038/s41598-025-86367-3MicroRNA-32-5p promotes the proliferation and metastasis of gastric cancer cellsChao Sun0Lai-gang Huang1Bing Leng2Yanting Guo3Chen Chen4Ruijie Lv5Yan Dong6Tian-tian Gao7De-qing Sun8Department of Pharmacy, The Second Hospital of Shandong UniversityDepartment of Rehabilitation Medicine, The Second Hospital of Shandong UniversityDepartment of Pharmacy, Shandong Provincial Hospital Affiliated to Shandong First Medical UniversityDepartment of Pharmacy, The First Affiliated Hospital of Shandong First Medical University & Shandong Provincial Qianfoshan HospitalDepartment of Pharmacy, The Second Hospital of Shandong UniversityDepartment of Pharmacy, The First Affiliated Hospital of Shandong First Medical University & Shandong Provincial Qianfoshan HospitalDepartment of Pharmacy, The Second Hospital of Shandong UniversityDepartment of Pharmacy, Shandong Provincial Hospital Affiliated to Shandong First Medical UniversityDepartment of Pharmacy, The Second Hospital of Shandong UniversityAbstract Gastric cancer (GC) is a huge threat to global health, there is no effective treatment or just delay the progression of advanced GC until now. Micro-RNAs were reported to participate in the progression of GC. Clonal formation, MTT, caspase-3 activity, sperm DNA fragmentation, flow cytometry assay, cell adhesion, transwell assays were performed to detect the functions of miR-32-5p or anti-miR-32-5p on the growth and metastasis of GC cells. Western blot, qRT-PCR, Co-immunoprecipitation, and luciferase reporter analysis were performed to explore the associated mechanisms. We established mouse tumor xenografts and mouse metastasis models to explore the role of miR-32-5p and anti-miR-32-5p in vivo. We found that miR-32-5p significantly promoting the proliferation and metastasis of GC cells at both in vitro and in vivo levels. The underlying mechanism maybe that miR-32-5p complementary paired with the 3′-UTR of DSC2, and inhibited the expression of DSC2. Furthermore, we found that DSC2 suppressed the transcription of Cyclin B1, and induced G2/M phase arrest through inhibiting the complex of β-catenin/TCF4 in nucleus. We concluded that miR-32-5p negatively regulated the DSC2 expression, might be a potential therapeutic targeting of cancers, most especially in GC.https://doi.org/10.1038/s41598-025-86367-3Desmocollin2microRNA-32-5pGastric cancerCyclin B1TCF4
spellingShingle Chao Sun
Lai-gang Huang
Bing Leng
Yanting Guo
Chen Chen
Ruijie Lv
Yan Dong
Tian-tian Gao
De-qing Sun
MicroRNA-32-5p promotes the proliferation and metastasis of gastric cancer cells
Scientific Reports
Desmocollin2
microRNA-32-5p
Gastric cancer
Cyclin B1
TCF4
title MicroRNA-32-5p promotes the proliferation and metastasis of gastric cancer cells
title_full MicroRNA-32-5p promotes the proliferation and metastasis of gastric cancer cells
title_fullStr MicroRNA-32-5p promotes the proliferation and metastasis of gastric cancer cells
title_full_unstemmed MicroRNA-32-5p promotes the proliferation and metastasis of gastric cancer cells
title_short MicroRNA-32-5p promotes the proliferation and metastasis of gastric cancer cells
title_sort microrna 32 5p promotes the proliferation and metastasis of gastric cancer cells
topic Desmocollin2
microRNA-32-5p
Gastric cancer
Cyclin B1
TCF4
url https://doi.org/10.1038/s41598-025-86367-3
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