ArticleLung2020
High Expression of CARM1 Inhibits Lung Cancer Progression by Targeting TP53 by Regulating CTNNB1.
Article in Lung, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 18 citations in OpenAlex.
- Article
- Integration analysis of microRNAs as potential biomarkers in early-stage lung adenocarcinoma: the diagnostic and therapeutic significance of miR-183-3p.Frontiers in oncology · 2024Article
- Dysregulation of arginine methylation in tumorigenesis.Frontiers in molecular biosciences · 2024Review
- Integrating UPLC-Q-Orbitrap MS with serum pharmacochemistry network and experimental verification to explore the pharmacological mechanisms ofFrontiers in pharmacology · 2024Article
- Inhibition of CARM1 suppresses proliferation of multiple myeloma cells through activation of p53 signaling pathway.Molecular biology reports · 2023Article
- Centipeda minima active components and mechanisms in lung cancer.BMC complementary medicine and therapies · 2023Article
- WDR5 promotes the tumorigenesis of oral squamous cell carcinoma via CARM1/β-catenin axis.Odontology · 2022Article
- Nine-gene signature and nomogram for predicting survival in patients with head and neck squamous cell carcinoma.Frontiers in genetics · 2022Article
- Exploration of Potential Targets and Mechanisms of Fisetin in the Treatment of Non-Small-Cell Lung Carcinoma via Network Pharmacology and In Vitro Validation.Evidence-based complementary and alternative medicine : eCAM · 2022Article
- Conditioned Media of Adipose-Derived Stem Cells Suppresses Sidestream Cigarette Smoke Extract Induced Cell Death and Epithelial-Mesenchymal Transition in Lung Epithelial Cells.International journal of molecular sciences · 2021Article
- LUNG Year in Review: 2020.Lung · 2021Article
- PRMT4 promotes hepatocellular carcinoma progression by activating AKT/mTOR signaling and indicates poor prognosis.International journal of medical sciences · 2021Article
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveTo explore the role of CARM1 in lung cancer (LC) and its relationship with TP53 and CTNNB1.
methodsLung cells H1299 and PC14 were randomly divided into six groups: ov-H1299, si-H1299, ov-PC14, si-PC14, Con-H1299, and Con-PC14. Transwell assay, plate clone formation assay, and flow cytometry were used to determine the migration, clone formation capacity, and apoptosis situation of LC cells in the six groups, respectively. Western blot assay was used to determine the protein expression of CARM1, TP53, and CTNNB1 in the six groups. CHIP assay was applied to analyze the combined characteristics of JUN and TP53 promoter. Co-immunoprecipitation was used to analyze the interaction between TP53 and CARM1/CTNNB1. Cox proportional hazard regression model was used to analyze the relevance between the expression of CARM1 and clinicopathological information of the patient. Kaplan-Meier plot was used to determine the relevance between CARM1 and patient survival.
resultsHigh expression of CARM1 inhibits the migration and proliferation of LC cells and promoted the apoptosis of LC cell. Overexpression of CARM1 promotes the expression of CARM1 and TP53, while decreases CTNNB1 expression. CARM1 supplementation of H1299 cells induced JUN aggregation on the TP53 promoter. TP53 and CARM1 protein/TP53 and CTNNB1 protein in H1299 cells were immunoprecipitated together. High expression of CARM1was negatively correlated with the degree of tumor metastasis. The survival period of patients with high expression CARM1 was greater than that of low expression.
conclusionOverexpression of CARM1 may inhibit the progression of LC by targeting TP53 via regulation CTNNB1.
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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.