ArticleCancer medicine2023
LncRNA DICER1-AS1 promotes colorectal cancer progression by activating the MAPK/ERK signaling pathway through sponging miR-650.
Article in Cancer medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 30 citations in OpenAlex.
- Pro-inflammatory and autophagic pathways in lung cancer: dysregulation of key genes ADINR, C/EBPα, CHAST, ATG5, IL-1B, and DICER1-AS1.Biochemistry and biophysics reports · 2026Article
- Gene Expression, Non-Coding RNA, and Circular RNA Alterations in Patients with T-Prolymphocytic Leukemia.Cancers · 2026Article
- Non-coding RNAs: modulators of signaling pathways and prognostic biomarkers in digestive system cancer.Molecular cancer · 2026Review
- Functions and mechanisms of miR-650 in human diseases.Frontiers in molecular biosciences · 2026Review
- Novel insights into lncRNAs as key regulators of post-translational modifications in cancer: mechanisms and therapeutic potential.Cellular oncology (Dordrecht, Netherlands) · 2025Review
- The macrophage galactose-type C-type lectin 1 receptor plays a major role in mediating colitis-associated colorectal cancer malignancy.Immunology and cell biology · 2025Article
- Bioinformatics analysis of lncRNA and mRNA differentially expressed in patients with cervical cancer.Frontiers in bioinformatics · 2025Article
- Long non‑coding RNAs as diagnostic and prognostic biomarkers for colorectal cancer (Review).Oncology letters · 2024Review
- RUNX transcription factors are essential in maintaining epididymal epithelial differentiation.Cellular and molecular life sciences : CMLS · 2024Article
- The functions and mechanisms of long non-coding RNA in colorectal cancer.Frontiers in oncology · 2024Review
- LncRNA DICER1-AS1 promotes colorectal cancer progression by activating the MAPK/ERK signaling pathway through sponging miR-650.Cancer medicine · 2023Article
- Orientin Reduces the Effects of Repeated Procedural Neonatal Pain in Adulthood: Network Pharmacology Analysis, Molecular Docking Analysis, and Experimental Validation.Pain research & management · 2023Article
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundColorectal cancer (CRC) is a disease with high morbidity and mortality rates globally. Long noncoding RNAs (lncRNAs) play a fundamental role in tumor progression, and increasing attention has been paid to their role in CRC. This study aimed to determine the function of lncRNA DICER1 antisense RNA 1 (DICER1-AS1) in CRC and confirm its potential regulatory mechanisms in CRC.
methodsThe publicly available dataset was used to assess DICER1-AS1 function and expression in CRC. RT-qPCR or western blot assays were performed to verify DICER1-AS1, miR-650, and mitogen-activated protein kinase 1 (MAPK1) expression in CRC cells or tissues. To determine the function of DICER1-AS1, we performed CCK-8, colony formation, transwell, cell cycle, and in vivo animal assays. Using RNA sequence analysis, luciferase reporter assays, and bioinformatics analysis, the connection between DICER1-AS1, MAPK1, and miR-650 was investigated.
resultsDICER1-AS1 was significantly upregulated in CRC tissue compared to normal colon tissue. High DICER1-AS1 expression suggested a poor prognosis in CRC patients. Functionally, upregulation of DICER1-AS1 effectively promoted CRC proliferation, migration, and invasion ex vivo and tumor progression in vivo. Mechanistically, DICER1-AS1 functions as a competitive endogenous RNA (ceRNA) that sponges miR-650 to upregulate MAPK1, promotes ERK1/2 phosphorylation, and sequentially activates the MAPK/ERK signaling pathway.
conclusionOur investigations found that upregulation of DICER1-AS1 activates the MAPK/ERK signaling pathway by sponging miR-650 to promote CRC progression, revealing a possible clinically significant biomarker and therapeutic target.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.