Evidence map›Paper›PMID 34945812›Full record

ArticleJournal of personalized medicine2021

Expression Dynamics of Heme Oxygenase-1 in Tumor Cells and the Host Contributes to the Progression of Tumors.

Jun Fang, Rayhanul Islam, Shanghui Gao, Cheng Zhang, Ryotaro Kunisaki, Shogo Sakaguchi, Naoya Honda, Jian-Rong Zhou, Kazumi Yokomizo

Open access · goldAbstract read
In one paragraph

Article in Journal of personalized medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.2field-weighted citation impact, top 46% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

5 citing papers in PubMed, 5 citations in OpenAlex.

  1. Heme-glycolysis interplay in oral squamous cell carcinoma: insights into SLC48A1 and GLUT1 expression across histological grades.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors at 2 institutions in 2 countries.

Jun FangLaboratory of Microbiology, Faculty of Pharmaceutical Sciences, Sojo University, Kumamoto 860-0082, Japan.
Rayhanul IslamLaboratory of Microbiology, Faculty of Pharmaceutical Sciences, Sojo University, Kumamoto 860-0082, Japan.ORCID 0000-0001-8621-2386
Shanghui GaoLaboratory of Microbiology, Faculty of Pharmaceutical Sciences, Sojo University, Kumamoto 860-0082, Japan.
Cheng ZhangDepartment of Toxicology, School of Public Health, Anhui Medical University, Hefei 230032, China.
Ryotaro KunisakiLaboratory of Microbiology, Faculty of Pharmaceutical Sciences, Sojo University, Kumamoto 860-0082, Japan.
Shogo SakaguchiLaboratory of Microbiology, Faculty of Pharmaceutical Sciences, Sojo University, Kumamoto 860-0082, Japan.
Naoya HondaLaboratory of Microbiology, Faculty of Pharmaceutical Sciences, Sojo University, Kumamoto 860-0082, Japan.
Jian-Rong ZhouLaboratory of Microbiology, Faculty of Pharmaceutical Sciences, Sojo University, Kumamoto 860-0082, Japan.
Kazumi YokomizoLaboratory of Microbiology, Faculty of Pharmaceutical Sciences, Sojo University, Kumamoto 860-0082, Japan.
Sojo University · JPAnhui Medical University · CN

Funding

Japan Society for the Promotion of Science 22700927, 25430162.
6 · The paper itself

Abstract

Heme oxygenase (HO-1) plays an important role in cellular protection against various stresses. The induction of HO-1 is an effective strategy for reactive oxygen species-related diseases, inflammatory diseases, as well as suppressing carcinogenesis. On the other hand, the high expression of HO-1 is now well known in many tumors. In this study, we investigated the dynamics of HO-1 expression in the host and the tumor. In the mouse sarcoma S180 solid tumor model and the rat hepatoma AH136B ascitic tumor model, HO-1 expression in the tumor, as indicated by the end product of HO-1 activation, i.e., carbon monoxide, gradually increased along with tumor growth. Over-expression of HO-1 expression in mouse colon cancer C26 tumor cells significantly promoted tumor growth as well as lung metastasis, whereas opposite results were found when the HO-1 expression was reduced in the cells. On the other hand, upregulating HO-1 levels in the host by using an HO-1 inducer protected the progression of the xenograft tumor in mice, whereas lowering HO-1 expression in the host with an HO-1 inhibitor showed accelerated tumor growth and lung metastasis after subcutaneous tumor xenograft inoculation. These findings strongly suggest that the balance of HO-1 levels in the host and the tumor cells is essential for the occurrence, progression, and prognosis of cancer. Maintenance of appropriately high HO-1 levels in the host is favorable for cancer prevention, whereas suppression of HO-1 in the tumor cells may thus become a therapeutic strategy for cancer.

Indexed as

carbon monoxidecarcinogenesisheme oxygenase-1tumor progression

Identifiers

PMID34945812
PMCPMC8704574
OpenAlexW4200251194

What OpenQuestion holds

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Registered trials

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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.