ArticlePloS one2013
Effect of chronic restraint stress on human colorectal carcinoma growth in mice.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
What it found
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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.
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Who cites it
44 citing papers in PubMed, 59 citations in OpenAlex.
- Unraveling the nexus in the neuro-neoplastic progression of colorectal cancer: Potential role of β2-adrenergic receptor (β2-AR).Journal of advanced research · 2026Review
- Pharmacological interventions targeting β-adrenoceptors in colorectal cancer: an evolving paradigm.Inflammopharmacology · 2025Review
- Investigating the Potential of Propranolol as an Anti-Tumor Agent in Colorectal Cancer Cell Lines.International journal of molecular sciences · 2025Article
- Acute stress causes sex-specific changes to ventral subiculum synapses, circuitry, and anxiety-like behavior.Nature communications · 2025Article
- Autonomic modulation of the immune response and implications for CNS malignancies.NPJ precision oncology · 2025Review
- Impact of Tumoral β2-Adrenergic Receptor Expression on Chemotherapeutic Response and Prognosis in Patients with Advanced Colorectal Cancer.Annals of surgical oncology · 2025Article
- Role of transforming growth factor-β1 pathway in angiogenesis induced by chronic stress in colorectal cancer.Cancer biology & therapy · 2024Article
- Multifaced Nature of Yohimbine-A Promising Therapeutic Potential or a Risk?International journal of molecular sciences · 2024Review
- Article
- Chronic Stress-induced Serotonin Impairs Intestinal Epithelial Cell Mitochondrial Biogenesis via the AMPK-PGC-1α Axis.International journal of biological sciences · 2024Article
- Norepinephrine/βJournal of breast cancer · 2023Article
- Interplay between stress and cancer-A focus on inflammation.Frontiers in physiology · 2023Review
- Chronic stress promotes colorectal cancer progression by enhancing glycolysis through β2-AR/CREB1 signal pathway.International journal of biological sciences · 2023Article
- A literature perspective on the pharmacological applications of yohimbine.Annals of medicine · 2022Review
- Anticancer potential of yohimbine in drug-resistant oral cancer KB-ChR-8-5 cells.Molecular biology reports · 2022Article
- Obesity and cancer-extracellular matrix, angiogenesis, and adrenergic signaling as unusual suspects linking the two diseases.Cancer metastasis reviews · 2022Review
- Effect of chronic stress on tumorigenesis and development.Cellular and molecular life sciences : CMLS · 2022Review
- Targeting tumor innervation: premises, promises, and challenges.Cell death discovery · 2022Review
- Using Mice to Model Human Disease: Understanding the Roles of Baseline Housing-Induced and Experimentally Imposed Stresses in Animal Welfare and Experimental Reproducibility.Animals : an open access journal from MDPI · 2022Review
- Contributing factors common to COVID‑19 and gastrointestinal cancer.Oncology reports · 2022Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Stress alters immunological and neuroendocrinological functions. An increasing number of studies indicate that chronic stress can accelerate tumor growth, but its role in colorectal carcinoma (CRC) progression is not well understood. The aim of this study is to investigate the effects of chronic restraint stress (CRS) on CRC cell growth in nude mice and the possible underlying mechanisms. In this study, we showed that CRS increased the levels of plasma catecholamines including epinephrine (E) and norepinephrine (NE), and stimulated the growth of CRC cell-derived tumors in vivo. Treatment with the adrenoceptor (AR) antagonists phentolamine (PHE, α-AR antagonist) and propranolol (PRO, β-AR antagonist) significantly inhibited the CRS-enhanced CRC cell growth in nude mice. In addition, the stress hormones E and NE remarkably enhanced CRC cell proliferation and viability in culture, as well as tumor growth in vivo. These effects were antagonized by the AR antagonists PHE and PRO, indicating that the stress hormone-induced CRC cell proliferation is AR dependent. We also observed that the β-AR antagonists atenolol (ATE, β1- AR antagonist) and ICI 118,551 (ICI, β2- AR antagonist) inhibited tumor cell proliferation and decreased the stress hormone-induced phosphorylation of extracellular signal-regulated kinases-1/2 (ERK1/2) in vitro and in vivo. The ERK1/2 inhibitor U0126 also blocked the function of the stress hormone, suggesting the involvement of ERK1/2 in the tumor-promoting effect of CRS. We conclude that CRS promotes CRC xenograft tumor growth in nude mice by stimulating CRC cell proliferation through the AR signaling-dependent activation of ERK1/2.
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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.