ArticleCancer management and research2023
TP63 Functions as a Tumor Suppressor Regulated by GAS5/miR-221-3p Signaling Axis in Human Non-Small Cell Lung Cancer Cells.
Article in Cancer management and research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
7 citing papers in PubMed, 11 citations in OpenAlex.
- Association between the TP63 and CIR1 polymorphisms and non-small cell lung cancer in Chinese population.Journal of cardiothoracic surgery · 2026Article
- Dysregulation of GAS5-miRNA-Mediated Signaling Pathways in Cancer Pathobiology: A Comprehensive Exploration of Pathways Influenced by this Axis.Biochemical genetics · 2025Review
- Epigenetic Regulation by lncRNA GAS5/miRNA/mRNA Network in Human Diseases.International journal of molecular sciences · 2025Review
- Anti-Cancer Bioactive Peptide Induces Apoptosis in Gastric Cancer Cells through TP53 Signaling Cascade.Protein and peptide letters · 2025Article
- An in vitro model of acute horizontal basal cell activation reveals gene regulatory networks underlying the nascent activation phase.Stem cell reports · 2024Article
- Research Progress of Long Non-Coding RNA in Tumor Drug Resistance: A New Paradigm.Drug design, development and therapy · 2024Review
- [Research Progress of LncRNA SNHGs in Regulating the Biological Behavior of Non-small Cell Lung Cancer].Zhongguo fei ai za zhi = Chinese journal of lung cancer · 2023Review
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Tumor protein p63 (TP63) has been proven to play a role as a tumor suppressor in some human cancers, including non-small cell lung cancer (NSCLC). This study aimed to investigate the mechanism of TP63 and analyze the underlying pathway dysregulating TP63 in NSCLC. Methods: RT-qPCR and Western blotting assays were used to determine gene expression in NSCLC cells. The luciferase reporter assay was performed to explore the transcriptional regulation. Flow cytometry was used to analyze the cell cycle and cell apoptosis. Transwell and CCK-8 assays were performed to test cell invasion and cell proliferation, respectively. Results: GAS5 interacted with miR-221-3p, and its expression was significantly reduced in NSCLC. GAS5, as a molecular sponge, upregulated the mRNA and protein levels of TP63 by inhibiting miR-221-3p in NSCLC cells. The upregulation of GAS5 inhibited cell proliferation, apoptosis, and invasion, which was partially reversed by the knockdown of TP63. Interestingly, we found that GAS5-induced TP63 upregulation promoted tumor chemotherapeutic sensitivity to cisplatin therapy in vivo and in vitro. Conclusion: Our results revealed the mechanism by which GAS5 interacts with miR-221-3p to regulate TP63, and targeting GAS5/miR-221-3p/TP63 may be a potential therapeutic strategy for NSCLC cells.
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