Evidence map›Paper›PMID 38999957›Full record

ArticleInternational journal of molecular sciences2024

Effects of High-Mobility Group Box-1 on Mucosal Immunity and Epithelial Differentiation in Colitic Carcinoma.

Takamitsu Sasaki, Rina Fujiwara-Tani, Yi Luo, Ruiko Ogata, Rika Sasaki, Ayaka Ikemoto, Yukiko Nishiguchi, Chie Nakashima, Shingo Kishi, Kiyomu Fujii and 3 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in International journal of molecular sciences, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
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

1 citing paper in PubMed.

  1. Review
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

13 authors.

Takamitsu SasakiDepartment of Molecular Pathology, Nara Medical University, 840 Shijo-Cho, Kashihara 634-8521, Nara, Japan.
Rina Fujiwara-TaniDepartment of Molecular Pathology, Nara Medical University, 840 Shijo-Cho, Kashihara 634-8521, Nara, Japan.
Yi LuoDepartment of Molecular Pathology, Nara Medical University, 840 Shijo-Cho, Kashihara 634-8521, Nara, Japan.
Ruiko OgataDepartment of Molecular Pathology, Nara Medical University, 840 Shijo-Cho, Kashihara 634-8521, Nara, Japan.
Rika SasakiDepartment of Molecular Pathology, Nara Medical University, 840 Shijo-Cho, Kashihara 634-8521, Nara, Japan.
Ayaka IkemotoDepartment of Molecular Pathology, Nara Medical University, 840 Shijo-Cho, Kashihara 634-8521, Nara, Japan.
Yukiko NishiguchiDepartment of Molecular Pathology, Nara Medical University, 840 Shijo-Cho, Kashihara 634-8521, Nara, Japan.
Chie NakashimaDepartment of Molecular Pathology, Nara Medical University, 840 Shijo-Cho, Kashihara 634-8521, Nara, Japan.
Shingo KishiPathology Laboratory, Research Institute, Tokushukai Nozaki Hospital, 2-10-50 Tanigawa, Daito 574-0074, Osaka, Japan.
Kiyomu FujiiDepartment of Molecular Pathology, Nara Medical University, 840 Shijo-Cho, Kashihara 634-8521, Nara, Japan.
Hitoshi OhmoriDepartment of Molecular Pathology, Nara Medical University, 840 Shijo-Cho, Kashihara 634-8521, Nara, Japan.
Naohide OuePathology Laboratory, Miyoshi Central Hospital, 10531 Higashi-Sakaya, Miyoshi 728-8502, Hiroshima, Japan.
Hiroki KuniyasuDepartment of Molecular Pathology, Nara Medical University, 840 Shijo-Cho, Kashihara 634-8521, Nara, Japan.ORCID 0000-0003-2298-8825

Funding

Ministry of Education, Culture, Sports, Science and Technology 19K16564Ministry of Education, Culture, Sports, Science and Technology 20K21659Ministry of Education, Culture, Sports, Science and Technology 21K06926Ministry of Education, Culture, Sports, Science and Technology 22K11396Ministry of Education, Culture, Sports, Science and Technology 23K19900
6 · The paper itself

Abstract

Abnormalities in mucosal immunity are involved in the onset and progression of ulcerative colitis (UC), resulting in a high incidence of colorectal cancer (CRC). While high-mobility group box-1 (HMGB1) is overexpressed during colorectal carcinogenesis, its role in UC-related carcinogenesis remains unclear. In the present study, we investigated the role of HMGB1 in UC-related carcinogenesis and sporadic CRC. Both the azoxymethane colon carcinogenesis and dextran sulfate sodium colitis carcinogenesis models demonstrated temporal increases in mucosal HMGB1 levels. Activated CD8+ cells initially increased and then decreased, whereas exhausted CD8+ cells increased. Additionally, we observed increased regulatory CD8+ cells, decreased naïve CD8+ cells, and decreased mucosal epithelial differentiation. In the in vitro study, HMGB1 induced energy reprogramming from oxidative phosphorylation to glycolysis in CD8+ cells and intestinal epithelial cells. Furthermore, in UC dysplasia, UC-related CRC, and hyperplastic mucosa surrounding human sporadic CRC, we found increased mucosal HMGB1, decreased activated CD8+ cells, and suppressed mucosal epithelial differentiation. However, we observed increased activated CD8+ cells in active UC mucosa. These findings indicate that HMGB1 plays an important role in modulating mucosal immunity and epithelial dedifferentiation in both UC-related carcinogenesis and sporadic CRC.

Indexed as

CD8-Positive T-LymphocytesCell DifferentiationColitis, UlcerativeHMGB1 ProteinImmunity, MucosalIntestinal MucosaAnimalsCarcinogenesisColorectal NeoplasmsEpithelial CellsHumansMaleMiceMice, Inbred C57BLHMGB1 ProteinHMGB1 protein, humancolitic carcinomaHMGB1mucosal immunitysporadic colorectal carcinomaulcerative colitis

Identifiers

PMID38999957
PMCPMC11241214

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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.