ArticleBiochemical genetics2023
Circ_0005615 Regulates the Progression of Colorectal Cancer Through the miR-873-5p/FOSL2 Signaling Pathway.
Article in Biochemical genetics, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
10 citing papers in PubMed, 12 citations in OpenAlex.
- Mechanism of miR-200b-3p-induced FOSL2 inhibition of endometrial cancer cell proliferation and metastasis.Scientific reports · 2025Article
- Exosomal circRNAs: Deciphering the novel drug resistance roles in cancer therapy.Journal of pharmaceutical analysis · 2025Review
- Crosstalk between non-coding RNAs and programmed cell death in colorectal cancer: implications for targeted therapy.Epigenetics & chromatin · 2025Review
- Exosomal CircRNAs: A Future Star in Colorectal Cancer.Current cancer drug targets · 2025Review
- Advances in extracellular vesicle (EV) biomarkers for precision diagnosis and therapeutic in colorectal cancer.Frontiers in oncology · 2025Review
- Roles of circRNAs in the progression of colorectal cancer: novel strategies for detection and therapy.Cancer gene therapy · 2024Review
- miR-873-5p Suppression Reinvigorates Aging Mesenchymal Stem Cells and Improves Cardiac Repair after Myocardial Infarction.ACS pharmacology & translational science · 2024Article
- Tumorigenic and tumoricidal properties of exosomes in cancers; a forward look.Cell communication and signaling : CCS · 2024Review
- Exosomal circRNAs in gastrointestinal cancer: Role in occurrence, development, diagnosis and clinical application (Review).Oncology reports · 2024Review
- Recent advances of exosomal circRNAs in cancer and their potential clinical applications.Journal of translational medicine · 2023Review
Corrections and comments
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Authors and funding
3 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
To determine the effects of circ_0005615 in CRC development and underneath mechanism. The expression levels of circ_0005615, microRNA-873-5p (miR-873-5p) and FOS-like antigen 2 (FOSL2) mRNA were determined by quantitative real-time polymerase chain reaction (qRT-PCR). The protein levels of exosome makers, proliferation-related makers and FOSL2 were detected by western blot or immunohistochemistry assay. Cell proliferation was evaluated by cell counting kit-8 (CCK-8) and cell colony formation assays. Cell migration and invasion were demonstrated by a transwell assay. Cell apoptosis was investigated by flow cytometry analysis. The binding relationship between miR-873-5p and circ_0005615 or FOSL2 was predicted by circular RNA interactome and targetscan online databases, respectively, and identified by dual-luciferase reporter assay. The impacts of circ_0005615 silencing on tumor formation were determined by in vivo tumor formation assay. Circ_0005615 expression was dramatically upregulated in serum exosomes of CRC patients compared with the control group. The CRC patients with a high circ_0005615 expression had a poor survival rate. Circ_0005615 and FOSL2 expressions were apparently increased, while miR-873-5p was decreased in CRC tissues or cells relative to control groups. Circ_0005615 knockdown inhibited cell proliferation, migration, and invasion, whereas promoted cell apoptosis in CRC; however, miR-873-5p inhibitor attenuated these impacts. Additionally, circ_0005615 acted as a sponge of miR-873-5p and miR-873-5p bound to FOSL2. FOSL2 overexpression restrained the effects of miR-873-5p mimic on CRC progression. Furthermore, circ_0005615 knockdown suppressed tumor growth in vivo. Circ_0005615 modulated CRC malignant progression by controlling FOSL2 expression through sponging miR-873-5p. This finding lays a foundation for the study on circRNA-mediated CRC therapy.
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Registered trials
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.