ArticleOncology letters2020
Aberrantly upregulated FAM83H-AS1 facilitates malignant progression of esophageal squamous cell carcinoma.
Article in Oncology letters, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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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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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
1 citing paper in PubMed.
- The emerging roles and mechanisms of FAM83H‑AS1 in cancer: Pathophysiology and therapeutic implications (Review).Oncology letters · 2025Review
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The biological roles of the newly identified long non-coding RNA family with sequence similarity 83 member H antisense 1 (FAM83H-AS1) in esophageal squamous cell carcinoma (ESCC) have remained largely elusive. In the present study, it was determined that, in comparison with paired para-tumorous tissues or normal esophageal epithelial cells, FAM83H-AS1 expression in cancer tissues and cell lines was markedly upregulated. Furthermore, FAM83H-AS1 expression was significantly elevated in patients with ESCC and lymph node metastasis or a late TNM stage, while no association with any other clinicopathological characteristics was detected. Furthermore, the overall and disease-free survival, as assessed by the Kaplan-Meier method, were significantly shortened in patients with high FAM83H-AS1 expression. A functional study then uncovered that knockdown of FAM83H-AS1 significantly suppressed the proliferation and migration of ESCC cells. The present results suggested that FAM83H-AS1 may facilitate the malignant progression of ESCC and may be utilized as a prognostic predictor and possibly a novel therapeutic target in ESCC that warrants further exploration.
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