ArticleHeliyon2023
LncRNA-HANR exacerbates malignant behaviors of cholangiocarcinoma cells through activating Notch pathway.
Article in Heliyon, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 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
7 citing papers in PubMed, 6 citations in OpenAlex.
- Mechanistic insights into the lncRNA-Notch signaling axis in tumors.Frontiers in cell and developmental biology · 2026Review
- Molecular mechanisms and genetic features of cholangiocarcinoma: implications for targeted therapeutic strategies.Precision clinical medicine · 2025Review
- LncRNA LUCAT1 as a prognostic biomarker in cholangiocarcinoma through targeting miR-141-3p: clinical and functional insights.Hereditas · 2025Article
- Construction of a novel cuproptosis-related gene signature and integrative analyses in cholangiocarcinoma.Heliyon · 2025Article
- Long Non-Coding RNA SNHG3 Promotes the Progression of Cholangiocarcinoma by Regulating the miR-151a-3p/STAT5a Axis.The Turkish journal of gastroenterology : the official journal of Turkish Society of Gastroenterology · 2024Article
- Classification of Long Non-Coding RNAs s Between Early and Late Stage of Liver Cancers From Non-coding RNA Profiles Using Machine-Learning Approach.Bioinformatics and biology insights · 2024Article
- Upregulation of long noncoding RNAsScience progressArticle
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Objectives: Cholangiocarcinoma (CHOL) is a malignant tumor from extrahepatic bile duct with poor prognosis. The critical roles of long non-coding RNAs (lncRNAs) in cancers including CHOL have been unveiled in recent decades. The present study was aimed to investigate the role and mechanism of a certain lncRNA, namely, hepatocellular carcinoma (HCC) associated long non-coding RNA (HANR) in CHOL. Methods: Reverse transcription quantitative polymerase chain reaction (RT-qPCR) was applied for detecting gene expression. Functional assays were done for assessing CHOL cell malignancy and mechanistic assays were conducted for analyzing correlation between HANR and Notch signal pathway, as well as the relation between HANR and Notch intracellular domain (NICD) in CHOL cells. Results: HANR was detected to be significantly overexpressed in CHOL cell lines. HANR silence inhibited cell proliferation, migration and stemness. Besides, HANR could positively regulate the Notch signaling pathway through modulating RBP-JK. HANR could bind to NICD and affect the transcriptional activity of RBP-JK. Furthermore, p-Notch1-NICD-r could wholly countervail the inhibitory effects of HANR silence on CHOL cell proliferation, migration and stemness. Conclusion: HANR could activate Notch pathway by regulating the RBP-JK transcriptional activity, thus contributing to exacerbated malignant behaviors of CHOL cells.
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