ArticleOncology letters2018
The impact of exogenous CO releasing molecule CORM-2 on inflammation and signaling of orthotopic lung cancer.
Article in Oncology letters, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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.
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
2 citing papers in PubMed, 10 citations in OpenAlex.
- Tumor Niche Influences the Activity and Delivery of Anticancer Drugs: Pharmacology Meets Chemistry.Pharmaceuticals (Basel, Switzerland) · 2025Review
- The potentials of carbon monoxide-releasing molecules in cancer treatment: An outlook from ROS biology and medicine.Redox biology · 2021Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The present study aimed to evaluate the therapeutic effect of CO-releasing molecule-2 (CORM-2) in an established mouse orthotopic lung cancer model and investigate the underlying mechanism associated with inflammation pathway. A total of 80 mice were randomly divided into two groups with 20 serving as a normal control and 60 used for the orthotopic lung cancer model. The tumor group was either untreated, or administrated with DMSO or CORM-2. The mice were sacrificed at day 7 and 14 post-treatment, and the body weight, and thymus and spleen indices were determined. Pathological analysis was performed with hematoxylin and eosin (HE) staining. Serous inflammatory factors were measured using an ELISA. The expression levels of eukaryotic translation initiation factor 4E, p70S6K and toll-like receptor-4 (TLR4) were quantified by reverse transcription-polymerase chain reaction. The effects of CORM-2 on the phosphoinositide 3-kinase (PI3K)/protein kinase B (Akt)/mammalian target of rapamycin (mTOR), TLR4/nuclear factor (NF)-κB signaling pathways were determined by western blotting. The body weight increased over time in the control group, while it significantly declined in tumor-bearing mice (P<0.05). CORM-2 treatment significantly increased body weight in comparison with the model and DSMO treatment groups (P<0.05). The thymus and spleen indices both reduced in the model and DMSO treatment groups, which was significantly rescued with CORM-2 administration (P<0.05). The HE staining results demonstrated few nodule formations, fibrous hyperplasia and extensive necrosis, which suggested overt inhibitory effects against cancer of CORM-2. The serous contents of tumor necrosis factor-α, interleukin (IL)-1β and IL-6 in the CORM-2 group was significantly lower compared with that in the model and DMSO groups (P<0.05). The ratio of phosphorylated (p-PI3K/PI3K, p-AKT/AKT, p-mTOR/mTOR, p-NF-κB-p65/NF-κB-p65 and expression of TLR4 significantly decreased in the CORM-2 group compared with the model and DMSO groups (P<0.05). To the best of our knowledge, the data in the present study demonstrated
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