ArticleMolecular medicine reports2016
Downregulation of thrombospondin-1 by DNA hypermethylation is associated with tumor progression in laryngeal squamous cell carcinoma.
Article in Molecular medicine reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 10 citations in OpenAlex.
- Proteomics reveals the regulation of ALG1 expression by lentivirus-mediated THBS1 overexpression and its mechanism in meibomian gland carcinoma.Oncology letters · 2025Article
- SWI/SNF ATPase silenced HLF potentiates lung metastasis in solid cancers.Nature communications · 2025Article
- scDiffCoAM: A complete framework to identify potential biomarkers for esophageal squamous cell carcinoma using scRNA-Seq data analysis.Journal of biosciences · 2024Article
- MicroRNA-3907 promotes the proliferation and migration of sebaceous gland carcinoma of the eyelid by targeting thrombospondin 1.Oncology letters · 2021Article
- Circulating methylated THBS1 DNAs as a novel marker for predicting peritoneal dissemination in gastric cancer.Journal of clinical laboratory analysis · 2021Article
- Long non-coding RNA BZRAP1-AS1 silencing suppresses tumor angiogenesis in hepatocellular carcinoma by mediating THBS1 methylation.Journal of translational medicine · 2019Article
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Thrombospondin‑1 (THBS‑1) has been demonstrated to have a complicated role in human cancer and to exert stimulatory and inhibitory effects in different types of tumors. DNA methylation, as the most frequent mechanism for gene silencing, has been widely investigated in regards to the development of tumors. However, the expression levels and methylation status of THBS‑1, and their roles in laryngeal squamous cell carcinoma (LSCC) remain to be elucidated. The present study detected downregulated THBS‑1 mRNA and protein expression levels in LSCC by using reverse transcription-quantitative polymerase chain reaction (PCR) and western blotting, while decreased expression levels of THBS‑1 mRNA and protein were significantly associated with lymph node metastasis and tumor‑node‑metastasis (TNM) stage. Furthermore, aberrant methylation of THBS‑1 was frequently observed in LSCC by methylation‑specific PCR, particularly in tumor tissues from lymph node metastasis or samples from cancer with advanced TNM stage. Furthermore, the current study demonstrated that downregulated expression of THBS‑1 in LSCC was consistent with aberrant methylation of this gene. Treatment with the DNA methyltransferase inhibitor 5-aza-2'-deoxy-cytidine in Hep‑2 cells induced demethylation of THBS-1, enhanced THBS‑1 expression, and inhibited the proliferative and invasive ability of Hep‑2 cells. Collectively, the results of the present study suggest that THBS‑1 may exert an inhibitory effect in the development of LSCC. Aberrant methylation was an important reason for the downregulation of THBS‑1 and was involved in the invasion and metastasis of LSCC. Demethylating agents may be effective candidates for the treatment of LSCC.
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