ArticleJournal of experimental & clinical cancer research : CR2018
Dysregulation of miR-6868-5p/FOXM1 circuit contributes to colorectal cancer angiogenesis.
Article in Journal of experimental & clinical cancer research : CR, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 24 citations in OpenAlex.
- Regulatory roles of non-coding and exosomal RNAs in colorectal cancer: spotlight on angiogenesis.Clinical and experimental medicine · 2025Review
- AREGMolecular medicine (Cambridge, Mass.) · 2025Article
- Down-regulation of microRNA-23a promotes pancreatic ductal adenocarcinoma initiation and progression by up-regulation of FOXM1 expression.Genes & diseases · 2024Article
- The role of FoxM1 in immune cells.Clinical and experimental medicine · 2023Review
- Footprints of microRNAs in Cancer Biology.Biomedicines · 2021Review
- Angiogenesis-related non-coding RNAs and gastrointestinal cancer.Molecular therapy oncolytics · 2021Review
- MicroRNAs and angiogenesis: a new era for the management of colorectal cancer.Cancer cell international · 2021Review
- Dysregulation of miR-23b-5p promotes cell proliferation via targeting FOXM1 in hepatocellular carcinoma.Cell death discovery · 2021Article
- Epigenetically modulated miR-1224 suppresses the proliferation of HCC through CREB-mediated activation of YAP signaling pathway.Molecular therapy. Nucleic acids · 2021Article
- Basic approaches, challenges and opportunities for the discovery of small molecule anti-tumor drugs.American journal of cancer research · 2021Review
- Long noncoding RNA HOXC-AS3 facilitates the progression of invasive mucinous adenocarcinomas of the lung via modulating FUS/FOXM1.In vitro cellular & developmental biology. Animal · 2020Article
- miR-877-5p Suppresses Gastric Cancer Cell Proliferation Through Targeting FOXM1.OncoTargets and therapy · 2020Article
- Angioregulatory microRNAs in Colorectal Cancer.Cancers · 2019Review
- Crosstalk between histone modification and DNA methylation orchestrates the epigenetic regulation of the costimulatory factors, Tim‑3 and galectin‑9, in cervical cancer.Oncology reports · 2019Article
- Based on Integrated Bioinformatics Analysis Identification of Biomarkers in Hepatocellular Carcinoma Patients from Different Regions.BioMed research international · 2019Article
- MiR-216b suppresses cell proliferation, migration, invasion, and epithelial-mesenchymal transition by regulating FOXM1 expression in human non-small cell lung cancer.OncoTargets and therapy · 2019Article
- Targeting Colorectal Cancer Stem Cells as an Effective Treatment for Colorectal Cancer.Technology in cancer research & treatmentReview
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Authors and funding
21 authors at 1 institution in 1 country.
Funding
Abstract
backgroundTranscription factor forkhead box M1 (FOXM1) is a crucial regulator in colorectal cancer (CRC) progression. However, the regulatory mechanisms causing dysregulation of FOXM1 in CRC remain unclear.
methodsDual-luciferase reporter assay was conducted to determine FOXM1 as miR-6868-5p target. The function of miR-6868-5p and FOXM1 in CRC angiogenesis was verified in vitro. Intratumoral injection model was constructed to explore the effect of miR-6868-5p on angiogenesis in vivo. Chromatin immunoprecipitation assays were used to assess direct binding of H3K27me3 to the miR-6868 promoter.
resultsThrough integrated analysis, we identified miR-6868-5p as the potent regulator of FOXM1. Overexpression of miR-6868-5p in CRC cells inhibited the angiogenic properties of co-cultured endothelial cells, whereas silencing of miR-6868-5p had opposite effects. In vivo delivery of miR-6868-5p blocked tumor angiogenesis in nude mice, resulting in tumor growth inhibition. Rescue of FOXM1 reversed the effect of miR-6868-5p on tumor angiogenesis. Further mechanistic study revealed that FOXM1 promoted the production of IL-8, which was responsible for the miR-6868-5p/FOXM1 axis-regulated angiogenesis. Reciprocally, FOXM1 inhibited miR-6868-5p expression through EZH2-mediated H3K27me3 on miR-6868-5p promoter, thus forming a feedback circuit. Clinically, the level of miR-6868-5p was downregulated in CRC tissues and inversely correlated with microvessel density as well as levels of FOXM1 and IL-8 in tumor specimens.
conclusionsTogether, these data identify miR-6868-5p as a novel determinant of FOXM1 expression and establish a miR-6868-5p/FOXM1 regulatory circuit for CRC angiogenesis, providing potential target for CRC treatment.
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