ArticleTranslational cancer research2021
Long non-coding RNA GHET1 promotes thyroid cancer cell proliferation and invasion.
Article in Translational cancer research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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3 citing papers in PubMed, 4 citations in OpenAlex.
- Exosomal LINC00900 deriving from mesenchymal stem cells inhibits cell growth in thyroid cancer via suppression of PTBP1.Journal of molecular histology · 2026Article
- The Interplay Between lncRNAs-microRNAs Network Dysregulation and Cellular Hallmarks of Thyroid Cancer.Cancers · 2025Review
- FOXP4-AS1 Inhibits Papillary Thyroid Carcinoma Proliferation and Migration Through the AKT Signaling Pathway.Frontiers in oncology · 2022Article
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundWe aimed to evaluate the role of long non-coding RNA (LncRNA) gastric carcinoma proliferation-enhancing transcript 1 (GHET1) on thyroid cancer (TC) behavior
methodsTC tissues and paired adjacent normal tissues were obtained after surgical excision from 43 patients with TC. The expression of LncRNA GHET1 was analyzed by real-time (RT) PCR. Human papillary thyroid cancer cell lines (TPC-1, BCPAP) were used to examine the role of LncRNA GHET1 in vitro. Cell proliferation was determined by CCK8 and cell colony formation assays. Transwell and wound-healing assays were used to detect the invasion and migration of thyroid cancer cells.
resultsOur results showed that LncRNA GHET1 was significantly more upregulated in TC tissues than in adjacent normal tissues. LncRNA GHET1 was also increased in thyroid cancer cell lines compared to normal thyroid cell lines. The upregulation of LncRNA GHET1 was significantly associated with tumor invasion, gender, and lymph node metastasis in patients with thyroid cancer. The
conclusionsLncRNA GHET1 dysregulation might be involved in the carcinogenesis of thyroid cancer. LncRNA GHET1 could be used as a potential molecular marker and molecular target for TC.
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