ArticleIranian journal of biotechnology2024
LncRNA U731166 Increases the Accumulation of TGFBR1 by Sponging miR-3607-3p in Esophageal Squamous-Cell Carcinomas (ESCC) to Promote Tumor Metastasis.
Article in Iranian journal of biotechnology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
2 citing papers in PubMed.
- Article
- Overexpression of LINC01354 predicts well prognosis and suppresses esophageal cancer progression.Scientific reports · 2025Article
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Authors and funding
11 authors.
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No grant is acknowledged in the PubMed record.
Abstract
Background: Long non-coding RNA (lncRNA) U731166 and microRNA (miR)-3607-3p are two ncRNAs with critical roles in cancer biology, while their involvement in esophageal squamous-cell carcinomas (ESCC) is unclear. We predicted that U731166 and miR-3607-3p might interact with each other. This study aimed to investigate their role and interaction in ESCC. Objectives: This study was therefore conducted to explore the involvement of U731166 and miR-3607-3p in ESCC, with a focus on the interaction between them. Materials and Methods: Paired ESCC and non-tumor tissue samples were recruited from 72 ESCC patients. By RT-Qpcr, level of U731166 and miR-3607-3p in paired tissues was measured. By RNA-RNA pulldown assay, the direct interaction between U731166 and miR-3607-3p was detected. U731166 overexpression or miR-3607-3p overexpression was performed to investigate their role in regulating the expression of each other. By RT-qPCR and Western blot analysis, the role of U731166 and miR-3607-3p in regulating the level of TGFBR1 was assessed. By Transwell assays, cell invasion and migration were analyzed. Results: Compared to non-tumor tissues, U731166 was highly upregulated in ESCC, while miR-3607-3p was downregulated in ESCC. U731166 and miR-3607-3p directly interacted with each other, but they are not closely correlated and did not regulate the level of each other. Moreover, U731166 reversed the role of miR-3607-3p in downregulating TGFBR1 and inhibiting cancer cell invasion and migration. U731166 and miR-3607-3p were closely associated with patients' tumor metastasis but not tumor size. Conclusion: U731166 may upregulate TGFBR1 by sponging miR-3607-3p in ESCC cells to promote tumor metastasis.
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