Article3 Biotech2022
KDM5A regulates the growth and gefitinib drug resistance against human lung adenocarcinoma cells.
Article in 3 Biotech, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 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
10 citing papers in PubMed, 11 citations in OpenAlex.
- Epigenetics in lung cancer precision medicine: from bench to bedside-a narrative review.Translational lung cancer research · 2026Review
- KDM5D expression is lost in cisplatin‑resistant neuroblastoma cells.Oncology reports · 2026Article
- The advancements in organoids: Potential and challenges in researching the esophagus and esophageal squamous cell carcinoma.Genes & diseases · 2026Review
- Review
- An Intrinsically Disordered Region of Histone Demethylase KDM5A Activates Catalysis Through Interactions With the Nucleosomal Acidic Patch and DNA.Journal of molecular biology · 2025Article
- Roles of KDM5 demethylases in therapeutic resistance of cancers.Epigenetics & chromatin · 2025Review
- An intrinsically disordered region of histone demethylase KDM5A activates catalysis through interactions with the nucleosomal acidic patch and DNA.bioRxiv : the preprint server for biology · 2025Article
- The KDM5A/HOXA5 axis regulates osteosarcoma progression via activating the Wnt/β-catenin pathway.European journal of medical research · 2025Article
- FOXP3 targets KIF5A to increase lactate production and promote docetaxel resistance in lung adenocarcinoma.Acta biochimica et biophysica Sinica · 2024Article
- Article
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 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
KDM5A, a histone demethylase, has been shown to be involved in several cancer-related process. The present study was undertaken to explore the role and therapeutic potential of KDM5A in human lung adenocarcinoma. The results of the qRT-PCR, immunohistochemistry, and western blotting showed significant upregulation of KDM5A expression in lung adenocarcinoma tissues and cell lines. The RNA interference-mediated silencing of KDM5A in lung adenocarcinoma cell line SK-LU-1 led to significant inhibition of in vitro cell proliferation via induction of apoptosis. The induction of apoptosis in SK-LU-1 lung adenocarcinoma cells was concomitant with upregulation of Bax and downregulation of Bcl-2 expression. In contrary, overexpression of KDM5A prompted the proliferation of SK-LU-1 lung adenocarcinoma cells. Interestingly, the SK-LU-1 cancer cells showed remarkably higher sensitivity to gefitinib under KDM5A transcriptional knockdown. Taken together, KDM5A is significantly upregulated in human lung adenocarcinoma and regulates the proliferation of the lung adenocarcinoma cells. These findings suggest potential of KDM5A to act as a therapeutic target for the management of human lung adenocarcinoma.
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.