ArticleBioengineered2022
Long non-coding RNA NCK1-AS1 is overexpressed in esophageal squamous cell carcinoma and predicts survival.
Article in Bioengineered, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 12 citations in OpenAlex.
- Interplay between TGF-β signaling and long non-coding RNAs in digestive system cancers: mechanisms and biological implications.Human cell · 2025Review
- Roles of long non-coding RNAs in oesophageal cancer pathogenesis.International journal of experimental pathology · 2025Review
- Osthole mitigates the myofibroblast properties in oral submucous fibrosis by suppressing the TGF-β/smad2 signaling pathway and NCK-AS1 expression.Journal of dental sciences · 2025Article
- NCK1 antisense RNA 1 (NCK1-AS1) exerts pro-fibrosis property in oral mucosa through modulation of miR-137/NCK1 axis.Journal of dental sciences · 2025Article
- Non‑coding RNA: A promising diagnostic biomarker and therapeutic target for esophageal squamous cell carcinoma (Review).Oncology letters · 2024Review
- Single Nucleotide Polymorphisms (SNPs) in the Shadows: Uncovering their Function in Non-Coding Region of Esophageal Cancer.Current pharmaceutical biotechnology · 2024Review
- The Role of the Transforming Growth Factor-β Signaling Pathway in Gastrointestinal Cancers.Biomolecules · 2023Review
- The Emerging Role of Long Non-Coding RNAs in Esophageal Cancer: Functions in Tumorigenesis and Clinical Implications.Frontiers in pharmacology · 2022Review
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Long noncoding RNAs have shown pivotal regulatory roles in tumorigenesis and progression. NCK1-AS1 promotes cervical cancer, while its involvement in esophageal cancer is hardly known. This study enrolled 52 esophageal squamous cell carcinoma (ESCC) patients (30 males and 22 females) at the average age of 56.4 ± 6.6 years in the range from 46 to 70 years, explored the involvement of NCK1-AS1 in ESCC, and analyzed the possible interaction between NCK1-AS1 and TGF-β signaling. Changes in gene expression were analyzed using RT-qPCR and Western blot. Interactions between gene expressions were analyzed using ESCC cells with transient transfections. Cell invasion and migration were analyzed using Transwell assays. Our data showed that plasma NCK1-AS1 was overexpressed in ESCC patients and positively correlated with NCK1-AS1 expression in tumor tissues but not in non-tumor tissues. Moreover, high plasma NCK1-AS1 levels were accompanied with poor survival. TGF-β1 expression level was also increased in tumor tissues compared to the adjacent normal tissues and positively correlated with NCK1-AS1 in tumor tissues. TGF-β1 overexpression in ESCC cells did not affect NCK1-AS1 expression, while NCK1-AS1 overexpression in ESCC cells upregulated TGF-β1. Moreover, TGF-β1 and NCK1-AS1 overexpression increased ESCC cell migration and invasion, while TGF-β inhibitor reduced the effects of NCK1-AS1 overexpression. Overall, NCK1-AS1 may promote ESCC by upregulating TGF-β1.
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