ArticleClinical and experimental medicine2022
Circular RNA circZCCHC6 contributes to tumorigenesis by regulating LPCAT1 via miR-433-3p in non-small cell lung cancer.
Article in Clinical and experimental medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 7 citations in OpenAlex.
- Association ofBiomedicines · 2025Article
- Exploring the Prognostic Potential of circSCORE in Patients with Relapsed/Refractory Mantle Cell Lymphoma.Genes · 2025Article
- Role of circular RNAs in lung cancer.Frontiers in genetics · 2024Review
- Multiplex Analysis of CircRNAs from Plasma Extracellular Vesicle-Enriched Samples for the Detection of Early-Stage Non-Small Cell Lung Cancer.Pharmaceutics · 2022Article
- MALAT1-miRNAs network regulate thymidylate synthase and affect 5FU-based chemotherapy.Molecular medicine (Cambridge, Mass.) · 2022Review
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Authors and funding
6 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Non-small cell lung cancer (NSCLC) is one of the leading causes of cancer-associated mortality worldwide. Circular RNA (circRNA) circZCCHC6 has been reported to be upregulated in the plasma from NSCLC patients. This study is designed to explore the role and mechanism of circZCCHC6 in NSCLC. CircZCCHC6, microRNA-433-3p (miR-433-3p), and lysophosphatidylcholine acyltransferase 1 (LPCAT1) level were determined by real-time quantitative polymerase chain reaction. Cell viability, cell cycle progression, migration, and invasion were assessed by 3-(4,5-dimethyl-2-thiazolyl)-2, 5-diphenyl-2-H-tetrazolium bromide (MTT), flow cytometry, wound healing, and transwell assays, severally. The binding relationship between miR-433-3p and circZCCHC6 or LPCAT1 was predicted by Circinteractome or Starbase, and then verified by a dual-luciferase reporter, RNA pull-down, or RNA Immunoprecipitation (RIP) assays. Protein levels of LPCAT1, Cyclin D1, E-cadherin, and Vimentin were examined by western blot assay. The biological role of circZCCHC6 on NSCLC tumor growth and epithelial-mesenchymal transition (EMT) was examined by the xenograft tumor model in vivo. CircZCCHC6 was highly expressed in NSCLC serum, tissues, and cells. Moreover, circZCCHC6 knockdown could repress cell viability, cell cycle progression, migration, invasion, and EMT in NSCLC cells in vitro. The mechanical analysis suggested that circZCCHC6 acted as a sponge of miR-433-3p to regulate LPCAT1 expression. CircZCCHC6 silencing hindered cell growth and EMT of NSCLC in vivo. CircZCCHC6 inhibited the progression of NSCLC cells partly by regulating the miR-433-3p/LPCAT1 axis, implying a promising therapeutic target for the NSCLC treatment.
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