Evidence map›Paper›PMID 40082457›Full record

ArticleScientific reports2025

Roles of C-reactive protein and LOX-1 on cancer and myeloid-derived suppressor cells in the progression of uterine cervical cancer.

Michihide Maeda, Seiji Mabuchi, Takashi Akazawa, Yu Mizote, Tomoyuki Sasano, Naoko Komura, Mina Sakata, Tsuyoshi Takiuchi, Shinya Matsuzaki, Tsuyoshi Hisa and 5 more

Abstract read
In one paragraph

Article in Scientific reports, 2025. 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. Article
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

15 authors.

Michihide MaedaDepartment of Obstetrics and Gynecology, Osaka University Graduate School of Medicine, 2-2 Yamadaoka, Suita, Osaka, 565-0871, Japan.
Seiji MabuchiDepartment of Gynecology, Osaka International Cancer Institute, 3-1-69 Otemae, Chuo-ku, Osaka, 540-0008, Japan. seijimabuchi@hyo-med.ac.jp.
Takashi AkazawaDepartment of Cancer Drug Discovery and Development, Research Center, Osaka International Cancer Institute, 3-1-69 Otemae, Chuo-ku, Osaka, 540-0008, Japan.
Yu MizoteDepartment of Cancer Drug Discovery and Development, Research Center, Osaka International Cancer Institute, 3-1-69 Otemae, Chuo-ku, Osaka, 540-0008, Japan.
Tomoyuki SasanoDepartment of Obstetrics and Gynecology, Osaka Saiseikai Nakatsu Hospital, 2-10-39 Shibata, Kita-ku, Osaka, 530-0012, Japan.
Naoko KomuraDepartment of Obstetrics and Gynecology, Kaizuka City Hospital, 3-10-20 Hori, Kaizuka, Osaka, 597-0015, Japan.
Mina SakataDepartment of Obstetrics and Gynecology, Osaka University Graduate School of Medicine, 2-2 Yamadaoka, Suita, Osaka, 565-0871, Japan.
Tsuyoshi TakiuchiDepartment of Obstetrics and Gynecology, Osaka University Graduate School of Medicine, 2-2 Yamadaoka, Suita, Osaka, 565-0871, Japan.
Shinya MatsuzakiDepartment of Obstetrics and Gynecology, Osaka University Graduate School of Medicine, 2-2 Yamadaoka, Suita, Osaka, 565-0871, Japan.
Tsuyoshi HisaDepartment of Gynecology, Osaka International Cancer Institute, 3-1-69 Otemae, Chuo-ku, Osaka, 540-0008, Japan.
Harumi NakamuraDepartment of Diagnostic Pathology and Cytology, Osaka International Cancer Institute, 3-1-69 Otemae, Chuo-ku, Osaka, 540-0008, Japan.
Tomoya EkawaDepartment of Cancer Drug Discovery and Development, Research Center, Osaka International Cancer Institute, 3-1-69 Otemae, Chuo-ku, Osaka, 540-0008, Japan.
Shoji KamiuraDepartment of Gynecology, Osaka International Cancer Institute, 3-1-69 Otemae, Chuo-ku, Osaka, 540-0008, Japan.
Tadashi KimuraDepartment of Obstetrics and Gynecology, Osaka University Graduate School of Medicine, 2-2 Yamadaoka, Suita, Osaka, 565-0871, Japan.
Hideaki TaharaDepartment of Cancer Drug Discovery and Development, Research Center, Osaka International Cancer Institute, 3-1-69 Otemae, Chuo-ku, Osaka, 540-0008, Japan.

Funding

Grant-in-Aid for General Scientific Research from the Ministry of Education, Culture, Sports, Science, and Technology of Japan 23K06666
6 · The paper itself

Abstract

We investigated clinical implications of CRP and its receptor, LOX-1, in cervical cancer progression and the underlying mechanisms. Clinical data from 121 patients with cervical cancer administered definitive radiotherapy were analyzed to investigate the relationship among pretreatment serum CRP levels, tumor LOX-1 expression, and treatment outcomes. Clinical samples, cervical cancer cell lines, and mouse xenograft models of cervical cancer were employed to elucidate the mechanisms for CRP-mediated progression of cervical cancer, focusing on LOX-1 expression on cancer and myeloid-derived suppressor (MDSCs) cells. Patients with elevated pretreatment CRP levels showed significantly shorter overall survival when their cervical tumor expressed LOX-1. In contrast, elevated pretreatment CRP levels had no prognostic relevance in patients with cervical tumors not expressing LOX-1. CRP treatment of LOX1-expressing cervical cancer cells induced ERK phosphorylation and stimulated cell proliferation in vitro. In vivo, CRP treatment promoted the progression of LOX-1-expressing cervical cancer. In vitro, it stimulated MDSC survival and augmented their suppressive activity. However, the tumor-promoting effects of CRP were minimal in tumors not expressing LOX-1. In conclusion, CRP facilitates progression of LOX-1-expressing cervical cancer by stimulating LOX-1 and its downstream effectors in cancer cells and MDSCs. Novel treatments targeting CRP or LOX-1 may be against LOX1-expressing cancer.

Indexed as

C-Reactive ProteinMyeloid-Derived Suppressor CellsScavenger Receptors, Class EUterine Cervical NeoplasmsAnimalsCell Line, TumorCell ProliferationDisease ProgressionFemaleHumansMiceMiddle AgedPrognosisC-Reactive ProteinOLR1 protein, humanScavenger Receptors, Class ECervical cancerC-reactive proteinInflammatory markerLOX-1MDSCsPrognosis

Identifiers

PMID40082457
PMCPMC11906838

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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.