ArticleAmerican journal of cancer research2022
Chronic stress promotes tumor immune evasion via the suppression of MHC-I expression and the upregulation of PD-L1.
Article in American journal of cancer research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.
What it found
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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.
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Who cites it
20 citing papers in PubMed, 1 synthesis or guideline pooled it, 16 citations in OpenAlex.
- Pooled it
- Long-term major histocompatibility complex class I suppression in astronauts and clinical implications.Communications biology · 2026Review
- Immune, molecular and genetic profiles of gastric signet ring cell carcinoma: Recent progress and future challenges.International journal of cancer · 2026Review
- The neuro-vascular-immune triad: the interactive network in the tumor microenvironment.Cell communication and signaling : CCS · 2026Review
- Neuro-Immune Crosstalk: Molecular Mechanisms, Biological Functions, Diseases, and Therapeutic Targets.MedComm · 2026Review
- The crosstalk between nerves and immunity: chronic stress as a driver of tumor progression.Frontiers in immunology · 2026Review
- Psychological distress as a putative host-state determinant of cancer immunotherapy response.Frontiers in immunology · 2026Review
- The neural niche in cancer: mechanistic insights into tumor-neuron-immune crosstalk and therapeutic opportunities.Frontiers in cell and developmental biology · 2026Review
- Neural regulation of immune evasion in breast cancer: a multiscale neuro-immune framework.Frontiers in immunology · 2026Review
- Beta-Blocker Use and Survival Outcomes in Pancreatic Cancer Patients: A Systematic Review and Meta-Analysis.Clinical Medicine Insights. Oncology · 2026Article
- [The TGF‑β/miR-23a-3p/IRF1 axis mediates immune escape of hepatocellular carcinoma by inhibiting major histocompatibility complex class I].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2025Article
- Chronic stress: a fourth etiology in tumorigenesis?Molecular cancer · 2025Review
- Single-cell RNA sequencing reveals the effects of mental stress on mouse mammary tumors and the tumor microenvironment.Cell death discovery · 2025Article
- Amino acid metabolism in glioblastoma pathogenesis, immune evasion, and treatment resistance.Cancer cell international · 2025Review
- Chronic Psychological Stress in Oncogenesis: Multisystem Crosstalk and Multimodal Interventions.Research (Washington, D.C.) · 2025Review
- The impact of β-blockers on outcomes of immune checkpoint inhibitors therapy in advanced lung cancer: a multicenter real-world study.Frontiers in immunology · 2025Article
- Role of β-adrenergic signaling and the NLRP3 inflammasome in chronic intermittent hypoxia-induced murine lung cancer progression.Respiratory research · 2024Article
- The Immune Landscape of Pheochromocytoma and Paraganglioma: Current Advances and Perspectives.Endocrine reviews · 2024Review
- Tumour microenvironment in pheochromocytoma and paraganglioma.Frontiers in endocrinology · 2023Review
- Non-pharmaceutical interventions to optimize cancer immunotherapy.Oncoimmunology · 2023Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chronic stress induces cancer initiation and progression via regulation of diverse cancer risk factors including immune evasion. Our previous research demonstrated that β-adrenergic blockade with propranolol almost completely reversed the accelerated tumor growth induced by chronic restraint stress, but the underlying mechanism of immune escape remains largely unknown. In the present study, a chronic restraint stress paradigm was applied to the H22 hepatocellular carcinoma (HCC) bearing mice to mimic the psychological stress. We observed that chronic restraint stress significantly promoted HCC growth and tumor escape from T cell surveillance. Chronic restraint stress reduced intratumor MHC-I expression and enhanced PD-L1 expression, whereas propranolol rectified the changes of MHC-I and PD-L1. Under chronic stress, the activated MAPK pathway suppressed MHC-I production by inactivating STAT1/IRF1 signaling pathway, and promoted PD-L1 translation by elevating eIF2α phosphorylation. These findings support the crucial role of β-adrenergic signaling cascade in the tumor escape from T cell surveillance under chronic restraint stress.
Indexed as
Identifiers
36504904PMC9729909W4311289600What 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.