ArticleMolecular oncology2023
KLF12 transcriptionally regulates PD-L1 expression in non-small cell lung cancer.
Article in Molecular oncology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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Who cites it
8 citing papers in PubMed, 10 citations in OpenAlex.
- M2 Microglia-Derived Exosomal miR-144-5p Attenuates White Matter Injury in Preterm Infants by Regulating the PTEN/AKT Pathway Through KLF12.Molecular biotechnology · 2026Article
- Enhancer hijacking drives FAM20C expression to promote papillary thyroid cancer progression.Cancer gene therapy · 2025Article
- Post-translational modifications of cancer immune checkpoints: mechanisms and therapeutic strategies.Molecular cancer · 2025Review
- KLF12 as a potential biomarker for lateral pelvic lymph node metastases in advanced rectal cancer.Cancer immunology, immunotherapy : CII · 2025Article
- Integrative analysis of genetic variability and functional traits in lung adenocarcinoma epithelial cells via single-cell RNA sequencing, GWAS, bayesian deconvolution, and machine learning.Genes & genomics · 2025Article
- KLF12 Aggravates Angiotensin II-Induced Cardiac Remodeling in Male Mice by Transcriptionally Inhibiting SMAD7.Journal of the American Heart Association · 2025Article
- Hexokinase HK3-mediated O-GlcNAcylation of EP300: a key regulator of PD-L1 expression and immune evasion in ccRCC.Cell death & disease · 2024Article
- Targeting T cell exhaustion: emerging strategies in non-small cell lung cancer.Frontiers in immunology · 2024Review
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 2 countries.
Funding
Abstract
Recent studies have pointed to the role of Krüpple-like factor 12 (KLF12) in cancer-associated processes, including cancer proliferation, apoptosis, and metastasis. However, the role of KLF12 in tumor immunity remains obscure. Here, we found that KLF12 expression was significantly higher in non-small cell lung cancer (NSCLC) cells with higher programmed death-ligand 1 (PD-L1) expression. Additionally, a positive correlation between KLF12 and PD-L1 was observed in clinical patient tumor tissues. By chromatin immunoprecipitation (ChIP) analysis, KLF12 was identified to bind to the CACCC motif of the PD-L1 promoter. Overexpression of KLF12 promoted PD-L1 transcription, whereas silencing of KLF12 inhibited PD-L1 transcription. Furthermore, signal transducer and activator of transcription 1 (STAT1)- and STAT3-triggered PD-L1 transcription was abolished in the absence of KLF12, and KLF12 knockdown weakened the binding of STAT1 and STAT3 to the PD-L1 promoter. Mechanistically, KLF12 physically interacted with P300, a histone acetyltransferase. In addition, KLF12 silencing reduced P300 binding to the PD-L1 promoter, which subsequently caused decreased acetylation of histone H3. PD-L1 transcription driven by KLF12 overexpression was eliminated by EP300 silencing. In immunocompetent mice, KLF12 knockout inhibited tumor growth and promoted infiltration of CD8
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