ArticleOpen medicine (Warsaw, Poland)2022
miR-455-5p enhances 5-fluorouracil sensitivity in colorectal cancer cells by targeting PIK3R1 and DEPDC1.
Article in Open medicine (Warsaw, Poland), 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.
- TCF7L2/DEPDC1 axis contributes to tumor progression by promoting cell proliferation, aerobic glycolysis, and immunosuppression in pancreatic cancer.Clinical and experimental medicine · 2026Article
- Multiple Machine Learning Models, Molecular Subtyping and Singlecell Analysis Identify PANoptosis-related Core Genes and their Association with Subtypes in Crohn's Disease.Current medicinal chemistry · 2025Article
- Cancer-AssociatedInternational journal of medical sciences · 2025Review
- Roles of DEPDC1 in various types of cancer (Review).Oncology letters · 2024Review
- Synthesis and Regulation of miRNA, Its Role in Oncogenesis, and Its Association with Colorectal Cancer Progression, Diagnosis, and Prognosis.Diagnostics (Basel, Switzerland) · 2024Review
- Bioinformatic Analyses and Integrated Machine Learning to Predict prognosis and therapeutic response Based on E3 Ligase-Related Genes in colon cancer.Journal of Cancer · 2024Article
- Research on the Regulatory Mechanism of Ginseng on the Tumor Microenvironment of Colorectal Cancer based on Network Pharmacology and Bioinformatics Validation.Current computer-aided drug design · 2024Article
- MicroRNAs (miRNAs): Novel potential therapeutic targets in colorectal cancer.Frontiers in oncology · 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
Our previous study has demonstrated that miR-455-5p was a tumor suppressor in colorectal cancer (CRC). This study aimed to investigate the role of miR-455-5p in 5-fluorouracil (5-Fu) in CRC. The expression of miR-455-5p, PIK3R1, and DEPDC1 was analyzed in HT-29 cells after treatment with different concentrations (0, 0.5, 2.5, and 12.5 μM) of 5-Fu. The effects of miR-455-5p on cell proliferation and apoptosis were analyzed by CCK-8 and flow cytometry. PIK3R1 and DEPDC1 were overexpressed to measure the mechanism of miR-455-5p on 5-Fu sensitivity. And the direct binding between miR-455-5p and DEPDC1 was detected by a dual-luciferase reporter assay. We found that miR-455-5p decreased, while PIK3R1 and DEPDC1 increased after 5-Fu treatment. miR-455-5p mimic significantly suppressed cell viability and elevated cell apoptosis in 5-Fu-treated HT-29 cells, whereas miR-455-5p inhibitor showed the opposite effects. Overexpression of PIK3R1 and DEPDC1 could attenuate the effects of miR-455-5p mimic on the viability and apoptosis of 5-Fu-treated cells. miR-455-5p could directly bind to DEPDC1 in HT-29 cells. In conclusion, miR-455-5p enhanced 5-Fu sensitivity by targeting PIK3R1 and DEPDC1 in CRC. This study provides a novel role of miR-455-5p in CRC and restoring miR-455-5p might be a therapeutic strategy to enhance chemosensitivity to 5-Fu.
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