ArticleOncology letters2020
AFAP1-AS1 induces cisplatin resistance in non-small cell lung cancer through PI3K/AKT pathway.
Article in Oncology letters, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 2 of them syntheses that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
19 citing papers in PubMed, 2 syntheses or guidelines pooled it, 26 citations in OpenAlex.
- High expression of AFAP1-AS1 is associated with poor prognosis of digestive system cancers: A meta-analysis.Medicine · 2022Pooled it
- Prognostic Value of EZH2 in Non-Small-Cell Lung Cancers: A Meta-Analysis and Bioinformatics Analysis.BioMed research international · 2020Pooled it
- TRIM33 Reverses Cisplatin Resistance in Non-Small Cell Lung Cancer by Regulating the PI3K/AKT Pathway via Ubiquitination-Mediated Degradation of LPCAT1.World journal of oncology · 2026Article
- Review
- Article
- Treating human cancer by targeting EZH2.Genes & diseases · 2025Review
- NAT10 Knockdown Improves Cisplatin Sensitivity in Non-Small Cell Lung Cancer by Inhibiting the TRIM44/PI3K/AKT Pathway.Thoracic cancer · 2025Article
- LncRNA AFAP1-AS1 Promotes Oral Squamous Cell Carcinoma Development by Ubiquitin-Mediated Proteolysis.International dental journal · 2024Article
- Current knowledge of antisense long non-coding RNA in the occurrence and prognosis of skull base tumors.Heliyon · 2024Review
- UBQLN4 promotes the proliferation and invasion of non-small cell lung cancer cell by regulating PI3K/AKT pathway.Journal of cancer research and clinical oncology · 2024Article
- The roles of EZH2 in cancer and its inhibitors.Medical oncology (Northwood, London, England) · 2023Review
- LncRNA AFAP1-AS1 Induces Gefitinib Resistance of Lung Adenocarcinoma Through the miR-653-5p/AGR2 Axis.Therapeutics and clinical risk management · 2023Article
- EZH2 Inhibition and Cisplatin as a Combination Anticancer Therapy: An Overview of Preclinical Studies.Cancers · 2022Review
- Metformin suppresses lung adenocarcinoma by downregulating long non-coding RNA (lncRNA) AFAP1-AS1 and secreted phosphoprotein 1 (SPP1) while upregulating miR-3163.Bioengineered · 2022Article
- PI3K/AKT signaling pathway as a critical regulator of Cisplatin response in tumor cells.Oncology research · 2021Review
- Silencing of LncRNA AFAP1-AS1 Inhibits Cell Proliferation in Oral Squamous Cancer by Suppressing CCNA2.Cancer management and research · 2021Article
- TP53-Activated lncRNA GHRLOS Regulates Cell Proliferation, Invasion, and Apoptosis of Non-Small Cell Lung Cancer by Modulating the miR-346/APC Axis.Frontiers in oncology · 2021Article
- Association of the Epithelial-Mesenchymal Transition (EMT) with Cisplatin Resistance.International journal of molecular sciences · 2020Review
- Diagnostic model of combined ceRNA and DNA methylation related genes in esophageal carcinoma.PeerJ · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cisplatin (DDP)-resistance in non-small cell lung carcinoma (NSCLC) severely influences the prognosis of affected patients. This study aims to uncover the potential role of AFAP1-AS1 in DDP-resistant NSCLC and the underlying mechanism. The expression level of AFAP1-AS1 in DDP-resistant NSCLC patients and DDP-resistant A549 cells (A549/DDP) was determined. Proliferative, cell cycle distribution, apoptotic, migratory and invasive changes in A549/DDP cells transfected with si-AFAP1-AS1 were assessed. Western blot analyses were conducted to examine the protein levels of phosphorylated protein kinase B (p-AKT), AKT, E-cadherin, N-cadherin, vimentin and snail in A549/DDP cells. Furthermore, the ubcellular distribution of AFAP1-AS1 was analyzed. Through RNA immunoprecipitation (RIP) assay, the interaction between AFAP1-AS1 and enhancer of zeste homolog 2 (EZH2) was explored. Finally, the regulatory effect of EZH2 on the PI3K/AKT pathway was investigated by western blot analysis. AFAP1-AS1 was upregulated in DDP-resistant NSCLC patients and A549/DDP cells. Transfection with si-AFAP1-AS1 attenuated the proliferative, migratory and invasive abilities, arrested cell cycle in G0/G1 phase, and stimulated apoptosis of A549/DDP cells. Silencing of AFAP1-AS1 upregulated E-cadherin and downregulated N-cadherin, vimentin and snail expression levels. Furthermore, AFAP1-AS1 was verified to interact with EZH2. The relative expression of EZH2 was reduced by transfection of A549/DDP cells with si-AFAP1-AS1. Silencing of EZH2 inhibited the activation of PI3K/AKT pathway. In conclusion, AFAP1-AS1 accelerates the proliferative and metastatic abilities of A549/DDP cells, whereas inhibits the apoptosis of A549/DDP cells, by interacting with EZH2 to activate the PI3K/AKT pathway; thus, inducing DDP resistance in NSCLC.
Indexed as
Identifiers
What OpenQuestion holds
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.