ArticleExperimental and therapeutic medicine2018
Downregulation of microRNA-193-3p inhibits the progression of intrahepatic cholangiocarcinoma cells by upregulating TGFBR3.
Article in Experimental and therapeutic medicine, 2018. 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, 14 citations in OpenAlex.
- MicroRNA-1 Suppresses Tumor Progression and UHRF1 Expression in Cholangiocarcinoma.International journal of molecular sciences · 2025Article
- Adipose Mesenchymal Stem Cell-Derived Exosomes Promote the Regeneration of Corneal Endothelium Through Ameliorating Senescence.Investigative ophthalmology & visual science · 2023Article
- A 13-Gene DNA Methylation Analysis Using Oral Brushing Specimens as an Indicator of Oral Cancer Risk: A Descriptive Case Report.Diagnostics (Basel, Switzerland) · 2022Article
- microRNA-193-3p attenuates myocardial injury of mice with sepsis via STAT3/HMGB1 axis.Journal of translational medicine · 2021Article
- The Role of microRNAs in Cholangiocarcinoma.International journal of molecular sciences · 2021Review
- Aspirin inhibits cholangiocarcinoma cell proliferation via cell cycle arrest in vitro and in vivo.International journal of oncology · 2021Article
- CRISPR/Cas9 uPAR Gene Knockout Results in Tumor Growth Inhibition, EGFR Downregulation and Induction of Stemness Markers in Melanoma and Colon Carcinoma Cell Lines.Frontiers in oncology · 2021Article
- Novel circular RNA expression profile of uveal melanoma revealed by microarray.Chinese journal of cancer research = Chung-kuo yen cheng yen chiu · 2018Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The aim of this study was to investigate the function of microRNA (miR)-193-3p in human intrahepatic cholangiocarcinoma (ICC) tissues and cells. To evaluate whether miR-193-3p was aberrantly upregulated, we used reverse transcription-quantitative polymerase chain reaction to detect the level of miR-193-3p in ICC tissues and ICC-9810 cells. The effects of miR-193-3p downregulation on ICC cell proliferation, migration and invasion were also measured by MTT, wound-healing and Transwell assays. Additionally, transforming growth factor-β receptor type 3 (TGFBR3) was investigated as a direct target of miR-193-3p by dual-luciferase reporter assays and western blot analyses. The results demonstrated that miR-193-3p was aberrantly upregulated in ICC tissues and cell lines. Furthermore, TGFBR3 was confirmed to be a target of miR-193-3p in ICC and was notably upregulated by miR-193-3p knockdown in the ICC-9810 cells. The knockdown of miR-193-3p also exerted direct inhibitory effects on the proliferation, migration and invasion of the ICC-9810 cells. Therefore, we present evidence that miR-193-3p plays a key role in promoting human ICC by regulating TGFBR3.
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