ArticleActa pharmacologica Sinica2022
The modulation of PD-L1 induced by the oncogenic HBXIP for breast cancer growth.
Article in Acta pharmacologica Sinica, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 21 citations in OpenAlex.
- Advances in Mechanism of Action and Efficacy of CBP/p300 Inhibitors in Different Subtypes of Breast Cancer.Molecules (Basel, Switzerland) · 2026Review
- LAMTOR5 promotes hepatoma growth in mice by disrupting LC3-p62-mediated autophagy and preventing p62 proteasome degradation.Acta pharmacologica Sinica · 2026Article
- Article
- Progress in understanding the regulatory mechanisms of immune checkpoint proteins PD-1 and PD-L1 expression.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2025Review
- Post-translational modifications of cancer immune checkpoints: mechanisms and therapeutic strategies.Molecular cancer · 2025Review
- Targeting PD-1 post-translational modifications for improving cancer immunotherapy.Cell insight · 2025Review
- Regulatory Mechanisms and Therapeutic Targeting of PD-L1 Trafficking and Stability in Cancer Immunotherapy.Cancers · 2025Review
- Revealing the Role of Beesioside O fromInternational journal of molecular sciences · 2025Article
- Exploring PANoptosis Related Novel Diagnostic Biomarkers and Potential Drugs for Sarcopenia based on Machine Learning and Experimental Validation.Current medicinal chemistry · 2025Article
- Berberine in combination with anti-PD-L1 suppresses hepatocellular carcinoma progression and metastasis via Erk signaling pathway.Annals of medicine and surgery (2012) · 2025Article
- Increased expression ofTranslational cancer research · 2024Article
- Research progress on oncoprotein hepatitis B X‑interacting protein (Review).Molecular medicine reports · 2024Review
- Targeting the PD-L1 cytoplasmic domain and its regulatory pathways to enhance cancer immunotherapy.Journal of molecular cell biology · 2024Review
- PTMs of PD-1/PD-L1 and PROTACs application for improving cancer immunotherapy.Frontiers in immunology · 2024Review
- Challenges Coexist with Opportunities: Spatial Heterogeneity Expression of PD-L1 in Cancer Therapy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Review
- Review
- Regulation of post-translational modification of PD-L1 and advances in tumor immunotherapy.Frontiers in immunology · 2023Review
- Method for detecting acetylated PD-L1 in cell lysates by immunoprecipitation and western blot analysis.PloS one · 2022Article
Corrections and comments
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Authors and funding
13 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Programmed death ligand-1 (PD-L1)/PD-1 checkpoint extensively serves as a central mediator of immunosuppression. A tumor-promoting role for abundant PD-L1 in several cancers is revealed. However, the importance of PD-L1 and how the PD-L1 expression is controlled in breast cancer remains obscure. Here, the mechanisms of controlling PD-L1 at the transcription and protein acetylation levels in promoting breast cancer growth are presented. Overexpressed PD-L1 accelerates breast cancer growth in vitro and in vivo. RNA-seq uncovers that PD-L1 can induce some target genes affecting many cellular processes, especially cancer development. In clinical breast cancer tissues and cells, PD-L1 and HBXIP are both increased, and their expressions are positively correlated. Mechanistic exploration identifies that HBXIP stimulates the transcription of PD-L1 through co-activating ETS2. Specifically, HBXIP induces PD-L1 acetylation at K270 site through interacting with acetyltransferase p300, leading to the stability of PD-L1 protein. Functionally, depletion of HBXIP attenuates PD-L1-accelerated breast tumor growth. Aspirin alleviates breast cancer via targeting PD-L1 and HBXIP. Collectively, the findings display new light into the mechanisms of controlling tumor PD-L1 and broaden the utility for PD-L1 as a target in breast cancer therapy.
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