ArticleBMC pulmonary medicine2022
C1QTNF6 regulated by miR-29a-3p promotes proliferation and migration in stage I lung adenocarcinoma.
Article in BMC pulmonary medicine, 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, 21 citations in OpenAlex.
- Review
- A Bioinformatics-Driven ceRNA Network in Stomach Adenocarcinoma: Identification of Novel Prognostic mRNA-miRNA-lncRNA Interactions.Medical sciences (Basel, Switzerland) · 2025Article
- Unveiling the origin and functions of diagnostic circulating microRNAs in lung cancer.British journal of cancer · 2025Article
- Comprehensive characterization of pathogenic missense CTRP6 variants and their association with cancer.BMC cancer · 2025Article
- Association of C1QTNF6 gene polymorphism with risk and clinical features of type 1 diabetes in Chinese: implications for ZnT8A and beta-cell function.Frontiers in immunology · 2025Article
- Article
- Article
- Novel genome-wide DNA methylation profiling reveals distinct epigenetic landscape, prognostic model and cellular composition of early-stage lung adenocarcinoma.Journal of translational medicine · 2024Article
- Siglec 15 as a biomarker or a druggable molecule for non-small cell lung cancer.Journal of cancer research and clinical oncology · 2023Review
- MiR-29a-3p: a potential biomarker and therapeutic target in colorectal cancer.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2023Review
- miR-29a-3p inhibits the malignant characteristics of non-small cell lung cancer cells by reducing the activity of the Wnt/β-catenin signaling pathway.Oncology letters · 2022Article
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
Abstract
objectiveC1QTNF6 has been implicated as an essential component in multiple cellular and molecular preliminary event, including inflammation, glucose metabolism, endothelial cell modulation and carcinogenesis. However, the biological process and potential mechanism of C1QTNF6 in lung adenocarcinoma (LUAD) are indefinite and remain to be elucidated. Therefore, we investigated the interaction among the traits of C1QTNF6 and LUAD pathologic process.
methodsRT-qPCR and western blot were conducted to determine the expression levels of C1QTNF6. RNA interference and overexpression of C1QTNF6 were constructed to identify the biological function of C1QTNF6 in cellular proliferative, migratory and invasive potentials in vitro. Dual-luciferase reporter assay was applied to identify the possible interaction between C1QTNF6 and miR-29a-3p. Moreover, RNA sequencing analysis of C1QTNF6 knockdown was performed to identify the potential regulatory pathways.
resultsC1QTNF6 was upregulated in stage I LUAD tissues compared with adjacent non-cancerous tissues. Concurrently, C1QTNF6 knockdown could remarkably inhibit cell proliferation, migratory and invasive abilities, while overexpression of C1QTNF6 presented opposite results. Additionally, miR-29a-3p may serve as an upstream regulator of C1QTNF6 and reduce the expression of C1QTNF6. Subsequent experiments showed that miR-29a-3p could decrease the cell mobility and proliferation positive cell rates, as well as reduce the migratory and invasive possibilities in LUAD cells via downregulating C1QTNF6. Moreover, RNA sequencing analysis demonstrated that the cytokine-cytokine receptor interaction pathway may participate in the process of C1QTNF6 regulating tumor progression.
conclusionOur study first demonstrated that downregulation of C1QTNF6 could inhibit tumorigenesis and progression in LUAD cells negatively regulated by miR-29a-3p. These consequences could reinforce our awareness and understanding of the underlying mechanism and provide a promising therapeutic target for LUAD.
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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 Socratic graph.