ArticleClinical & experimental metastasis2019
Promoter hypermethylation-mediated downregulation of tumor suppressor gene SEMA3B and lncRNA SEMA3B-AS1 correlates with progression and prognosis of esophageal squamous cell carcinoma.
Article in Clinical & experimental metastasis, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 36 citations in OpenAlex.
- Advances in semaphorin 3B research in tumors (Review).Molecular and clinical oncology · 2026Review
- Aberrant DNA Methylation in Esophageal Squamous Cell Carcinoma and its Clinical Implications in Systemic Chemotherapy.International journal of medical sciences · 2025Review
- Ten Hypermethylated lncRNA Genes Are Specifically Involved in the Initiation, Progression, and Lymphatic and Peritoneal Metastasis of Epithelial Ovarian Cancer.International journal of molecular sciences · 2024Article
- SEMA3B inhibits TGFβ-induced extracellular matrix protein production and its reduced levels are associated with a decline in lung function in IPF.American journal of physiology. Cell physiology · 2024Article
- Single Nucleotide Polymorphisms (SNPs) in the Shadows: Uncovering their Function in Non-Coding Region of Esophageal Cancer.Current pharmaceutical biotechnology · 2024Review
- High methylation of the same promoter of lncRNAEpigenomics · 2024Article
- scDiffCoAM: A complete framework to identify potential biomarkers for esophageal squamous cell carcinoma using scRNA-Seq data analysis.Journal of biosciences · 2024Article
- Article
- Mechanisms of radiotherapy resistance and radiosensitization strategies for esophageal squamous cell carcinoma.Molecular cancer · 2023Review
- Regulatory Roles of Noncoding RNAs in the Progression of Gastrointestinal Cancers and Health Disparities.Cells · 2022Review
- A Pleiotropic Role of Long Non-Coding RNAs in the Modulation of Wnt/β-Catenin and PI3K/Akt/mTOR Signaling Pathways in Esophageal Squamous Cell Carcinoma: Implication in Chemotherapeutic Drug Response.Current oncology (Toronto, Ont.) · 2022Review
- A genomic instability-related lncRNA model for predicting prognosis and immune checkpoint inhibitor efficacy in breast cancer.Frontiers in immunology · 2022Article
- Construction of prognostic signature of breast cancer based on N7-Methylguanosine-Related LncRNAs and prediction of immune response.Frontiers in genetics · 2022Article
- Establishment and Analysis of a Prognostic Model of Autophagy-Related lncRNAs in ESCA.BioMed research international · 2022Article
- Autophagy related long non-coding RNA and breast cancer prognosis analysis and prognostic risk model establishment.Annals of translational medicine · 2022Article
- The lncRNA SEMA3B-AS1/HMGB1/FBXW7 Axis Mediates the Peritoneal Metastasis of Gastric Cancer by Regulating BGN Protein Ubiquitination.Oxidative medicine and cellular longevity · 2022Article
- Long Non-Coding RNA in Esophageal Cancer: A Review of Research Progress.Pathology oncology research : POR · 2022Review
- Upregulation of cervical carcinoma expressed PCNA regulatory long non-coding RNA promotes esophageal squamous cell carcinoma progression.Oncology letters · 2020Article
- Identification and validation of stemness-related lncRNA prognostic signature for breast cancer.Journal of translational medicine · 2020Article
- Aberrant DNA Methylation in Esophageal Squamous Cell Carcinoma: Biological and Clinical Implications.Frontiers in oncology · 2020Review
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Frequent deletions of tumor-suppressor genes at chromosome 3p21.3 have been detected in esophageal squamous cell carcinoma (ESCC). As a candidate tumor suppressor gene, semaphorin 3B (SEMA3B) is located at 3p21.3 and is frequently inactivated in several tumors. However, the role and inactivation mechanisms of SEMA3B and its antisense long non-coding RNA (lncRNA) SEMA3B-AS1 in the carcinogenesis of ESCC have not been fully elucidated. The present study was conducted to investigate the role, epigenetic inactivation mechanisms, and prognostic value of SEMA3B and SEMA3B-AS1 in ESCC tumorigenesis and prognosis. Frequent downregulation of SEMA3B and SEMA3B-AS1 was detected in esophageal cancer cells and ESCC tissues, and the expression level of SEMA3B and SEMA3B-AS1 in ESCC tissues was correlated with TNM stage and lymph node metastasis. SEMA3B and SEMA3B-AS1 shared the same CpG island in the promoter region and the expression of both genes might be regulated by the promoter methylation status. Furthermore, transcription factor Sp1 activated SEMA3B or SEMA3B-AS1 transcription and the promoter hypermethylation of SEMA3B and SEMA3B-AS1 influenced Sp1 binding ability. Moreover, over-expression of SEMA3B and SEMA3B-AS1 suppressed the viability and invasion of esophageal cancer cells in vitro. SEMA3B-AS1 influenced the protein expression of SEMA3B. SEMA3B or SEMA3B-AS1 expression and promoter methylation status were correlated with ESCC patients' survival. Thus, these findings suggest that SEMA3B and SEMA3B-AS1 may act as tumor suppressors and may serve as potential targets for antitumor therapy.
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