DNMT1 blocks SOX21-repressed CKS2 transcription to promote gastric cancer progression

Abstract Background The dysregulation of SOXs is related to tumor invasion, metastasis, proliferation, apoptosis, and epithelial-mesenchymal transition. This research sought to investigate the function and mechanisms of SOX21 in gastric cancer (GC). Methods Multiple databases were included to determ...

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Main Authors: Jie Wei, Song Xue, Xinglong Du, Yuanfei Dai, Yuting Ji, Guangsi He
Format: Article
Language:English
Published: BMC 2025-07-01
Series:BMC Cancer
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Online Access:https://doi.org/10.1186/s12885-025-14577-z
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author Jie Wei
Song Xue
Xinglong Du
Yuanfei Dai
Yuting Ji
Guangsi He
author_facet Jie Wei
Song Xue
Xinglong Du
Yuanfei Dai
Yuting Ji
Guangsi He
author_sort Jie Wei
collection DOAJ
description Abstract Background The dysregulation of SOXs is related to tumor invasion, metastasis, proliferation, apoptosis, and epithelial-mesenchymal transition. This research sought to investigate the function and mechanisms of SOX21 in gastric cancer (GC). Methods Multiple databases were included to determine the hub transcription factors in GC. In addition, RT-qPCR and Western blot were used to validate gene expression in tissues from GC patients. CCK-8, EdU, colony formation, wound healing, Transwell assays, and a xenograft tumor model were used to determine the function of SOX21 in GC. The targets of SOX21 were predicted and verified using ChIP, dual-luciferase reporter, and functional assays. SOX21 DNA methylation in GC cells was determined by qMSP. Rescue experiments were carried out in GC cells with DNMT1 silencing alone or in combination with SOX21 silencing. Results SOX21 was downregulated in GC tissues and cells. Ectopic expression of SOX21 inhibited cell growth, invasion, and migration, and induced apoptosis of GC cells. CKS2 was a target of SOX21, and overexpression of CKS2 promoted cell viability and mobility in GC cells overexpressing SOX21. The downregulation of SOX21 was related to the DNA hypermethylation catalyzed by DNMT1. The silencing of SOX21, by contrast, overturned the anti-tumor effects of sh-DNMT1 in vitro and in vivo. Conclusion Our data showed that DNMT1 overexpression upregulated CKS2 expression via hypermethylation of SOX21, thus promoting GC cell proliferation and growth, indicating that the DNMT1/SOX21/CKS2 axis could be a target for GC treatment.
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spelling doaj-art-e081be659e98403783a3f9b05da2ba212025-08-20T03:05:09ZengBMCBMC Cancer1471-24072025-07-0125111810.1186/s12885-025-14577-zDNMT1 blocks SOX21-repressed CKS2 transcription to promote gastric cancer progressionJie Wei0Song Xue1Xinglong Du2Yuanfei Dai3Yuting Ji4Guangsi He5Department of Oncology, The Affiliated Chuzhou Hospital of Anhui Medical University (The First People’s Hospital of Chuzhou)Department of Oncology, The Affiliated Chuzhou Hospital of Anhui Medical University (The First People’s Hospital of Chuzhou)Department of Oncology, The Affiliated Chuzhou Hospital of Anhui Medical University (The First People’s Hospital of Chuzhou)Department of Oncology, The Affiliated Chuzhou Hospital of Anhui Medical University (The First People’s Hospital of Chuzhou)Department of Oncology, The Affiliated Chuzhou Hospital of Anhui Medical University (The First People’s Hospital of Chuzhou)Department of Oncology, The Affiliated Chuzhou Hospital of Anhui Medical University (The First People’s Hospital of Chuzhou)Abstract Background The dysregulation of SOXs is related to tumor invasion, metastasis, proliferation, apoptosis, and epithelial-mesenchymal transition. This research sought to investigate the function and mechanisms of SOX21 in gastric cancer (GC). Methods Multiple databases were included to determine the hub transcription factors in GC. In addition, RT-qPCR and Western blot were used to validate gene expression in tissues from GC patients. CCK-8, EdU, colony formation, wound healing, Transwell assays, and a xenograft tumor model were used to determine the function of SOX21 in GC. The targets of SOX21 were predicted and verified using ChIP, dual-luciferase reporter, and functional assays. SOX21 DNA methylation in GC cells was determined by qMSP. Rescue experiments were carried out in GC cells with DNMT1 silencing alone or in combination with SOX21 silencing. Results SOX21 was downregulated in GC tissues and cells. Ectopic expression of SOX21 inhibited cell growth, invasion, and migration, and induced apoptosis of GC cells. CKS2 was a target of SOX21, and overexpression of CKS2 promoted cell viability and mobility in GC cells overexpressing SOX21. The downregulation of SOX21 was related to the DNA hypermethylation catalyzed by DNMT1. The silencing of SOX21, by contrast, overturned the anti-tumor effects of sh-DNMT1 in vitro and in vivo. Conclusion Our data showed that DNMT1 overexpression upregulated CKS2 expression via hypermethylation of SOX21, thus promoting GC cell proliferation and growth, indicating that the DNMT1/SOX21/CKS2 axis could be a target for GC treatment.https://doi.org/10.1186/s12885-025-14577-zGastric cancerDNMT1SOX21CKS2Hypermethylation
spellingShingle Jie Wei
Song Xue
Xinglong Du
Yuanfei Dai
Yuting Ji
Guangsi He
DNMT1 blocks SOX21-repressed CKS2 transcription to promote gastric cancer progression
BMC Cancer
Gastric cancer
DNMT1
SOX21
CKS2
Hypermethylation
title DNMT1 blocks SOX21-repressed CKS2 transcription to promote gastric cancer progression
title_full DNMT1 blocks SOX21-repressed CKS2 transcription to promote gastric cancer progression
title_fullStr DNMT1 blocks SOX21-repressed CKS2 transcription to promote gastric cancer progression
title_full_unstemmed DNMT1 blocks SOX21-repressed CKS2 transcription to promote gastric cancer progression
title_short DNMT1 blocks SOX21-repressed CKS2 transcription to promote gastric cancer progression
title_sort dnmt1 blocks sox21 repressed cks2 transcription to promote gastric cancer progression
topic Gastric cancer
DNMT1
SOX21
CKS2
Hypermethylation
url https://doi.org/10.1186/s12885-025-14577-z
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