ArticleThoracic cancer2022
Knockdown of circ-RAD23B inhibits non-small cell lung cancer progression via the miR-142-3p/MAP4K3 axis.
Article in Thoracic cancer, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 13 citations in OpenAlex.
- Crosstalk between circRNAs and the MAPK signaling pathway in cancer progression.Discover oncology · 2026Review
- Carbon ion irradiation conquers the radioresistance by inducing complex DNA damage and apoptosis in U251 human glioblastomas cells.Medical oncology (Northwood, London, England) · 2025Article
- RAD23B Promotes Colorectal Cancer Metastasis via the Talin1/Integrin/PI3K/AKT/MMP9 Axis.Oncology research · 2025Article
- Review
- Circular RNAs in lung cancer: implications for preventing therapeutic resistance.EBioMedicine · 2024Review
- Regulation of Angiogenesis by Non-Coding RNAs in Cancer.Biomolecules · 2024Review
- AutoEdge-CCP: A novel approach for predicting cancer-associated circRNAs and drugs based on automated edge embedding.PLoS computational biology · 2024Article
- Circular RNAs-mediated angiogenesis in human cancers.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2023Review
- Non-coding RNAs in lung cancer: molecular mechanisms and clinical applications.Frontiers in oncology · 2023Review
- Circular RNA_0001187 participates in the regulation of ulcerative colitis development via upregulating myeloid differentiation factor 88.Bioengineered · 2022Article
- Knockdown of circ-RAD23B inhibits non-small cell lung cancer progression via the miR-142-3p/MAP4K3 axis.Thoracic cancer · 2022Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe development of non-small cell lung cancer (NSCLC) is associated with the deregulation of circRNAs. The objective of this study was to investigate the effects of circ-RAD23B in NSCLC.
methodsCirc-RAD23B expression, miR-142-3p and MAP4K3 was detected by qPCR. Cell proliferation was investigated by CCK-8 assay and colony formation assay. Cell migration and invasion were assessed by transwell assay. Angiogenesis ability was assessed by tube formation assay. Cell cycle distribution and cell apoptosis were monitored by flow cytometry. The predicted binding relationship between miR-142-3p and circ-RAD23B or MAP4K3 was verified by dual-luciferase reporter assay. The protein level of MAP4K3 was detected by western blot. Animal models were established to determine the role of circ-RAD23B in vivo.
resultsCirc-RAD23B was shown to be upregulated in NSCLC tissues and cells. Knockdown of circ-RAD23B inhibited proliferation, migration, invasion, angiogenesis and promoted cell cycle arrest and apoptosis in NSCLC cells, and circ-RAD23B knockdown also impeded tumor growth in vivo. Circ-RAD23B acted as miR-142-3p sponge to inhibit miR-142-3p expression and thus enrich the expression of MAP4K3, a target of miR-142-3p. Rescue experiments presented that miR-142-3p inhibition reversed the effects of circ-RAD23B knockdown, and MAP4K3 overexpression abolished the effects of miR-142-3p restoration. In addition, we found that circ-RAD23B knockdown led to decreased phosphorylation expression of ERK1/2, JNK and p38, three key groups of the MAPK signaling pathway.
conclusionsCirc-RAD23B knockdown inhibited NSCLC development by regulating the miR-142-3p/MAP4K3 axis, which might be associated with the inactivation of the MAPK signaling pathway.
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