ArticleOncogene2015
Selective killing of lung cancer cells by miRNA-506 molecule through inhibiting NF-κB p65 to evoke reactive oxygen species generation and p53 activation.
Article in Oncogene, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers.
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
65 citing papers in PubMed, 108 citations in OpenAlex.
- Pathogenic role and therapeutic targets of nuclear factor-κB signaling pathway in cancer (Review).Oncology letters · 2025Review
- Hsa_circ_0071271 affected the progression of non-small cell lung cancer through miR-23a-5p.Hereditas · 2025Article
- The crosstalk between non-coding RNAs and oxidative stress in cancer progression.Genes & diseases · 2025Review
- DeepLCRmiRNA: A Hybrid Neural Network Approach for Identifying Lung Cancer-Associated miRNAs.Current gene therapy · 2025Article
- Therapeutic potential of microRNA-506 in cancer treatment: mechanisms and therapeutic implications.Frontiers in oncology · 2025Review
- MicroRNAs in metabolism for precision treatment of lung cancer.Cellular & molecular biology letters · 2024Review
- MicroRNAs as Regulators of Radiation-Induced Oxidative Stress.Current issues in molecular biology · 2024Review
- Stable Dual miR-143 and miR-506 Upregulation Inhibits Proliferation and Cell Cycle Progression.International journal of molecular sciences · 2024Article
- Advances in the Study of Non-Coding RNA in the Signaling Pathway of Pulmonary Fibrosis.International journal of general medicine · 2024Review
- MiREx: mRNA levels prediction from gene sequence and miRNA target knowledge.BMC bioinformatics · 2023Article
- Altered MicroRNA Maturation in Ischemic Hearts: Implication of Hypoxia on XPO5 and DICER1 Dysregulation and RedoximiR State.Antioxidants (Basel, Switzerland) · 2023Article
- miRNAs Participate in the Regulation of Oxidative Stress-Related Gene Expression in Endometrioid Endometrial Cancer.International journal of molecular sciences · 2022Article
- Article
- ECSIT inhibits cell death to increase tumor progression and metastasis via p53 in human breast cancer.Translational cancer research · 2022Article
- An Immune-Related Genetic Feature Depicted the Heterogeneous Nature of Lung Adenocarcinoma and Squamous Cell Carcinoma and Their Distinctive Predicted Drug Responses.Oxidative medicine and cellular longevity · 2022Article
- MicroRNA-506-3p inhibits ovarian cancer metastasis by down-regulating the expression of EZH2.Journal of Cancer · 2022Article
- GSDMD-mediated pyroptosis: a critical mechanism of diabetic nephropathy.Expert reviews in molecular medicine · 2021Review
- HNRNPA2B1 as a trigger of RNA switch modulates the miRNA-mediated regulation of CDK6.iScience · 2021Article
- Interaction of microRNAs with sphingosine kinases, sphingosine-1 phosphate, and sphingosine-1 phosphate receptors in cancer.Discover oncology · 2021Review
- MicroRNA-499 serves as a sensitizer for lung cancer cells to radiotherapy by inhibition of CK2α-mediated phosphorylation of p65.Molecular therapy oncolytics · 2021Article
5 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
15 authors at 7 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The tumor suppressor p53, nuclear factor-κB (NF-κB) and reactive oxygen species (ROS) have crucial roles in tumorigenesis, although the mechanisms of cross talk between these factors remain largely unknown. Here we report that miR-506 upregulation occurs in 83% of lung cancer patients (156 cases), and its expression highly correlates with ROS. Ectopic expression of miR-506 inhibits NF-κB p65 expression, induces ROS accumulation and then activates p53 to suppress lung cancer cell viability, but not in normal cells. Interestingly, p53 promotes miR-506 expression level, indicating that miR-506 mediates cross talk between p53, NF-κB p65 and ROS. Furthermore, we demonstrated that miR-506 mimics inhibited tumorigenesis in vivo, implicating that miR-506 might be a potential therapeutic molecule for selective killing of lung cancer cells.
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.