Evidence map›Paper›PMID 40596619›Full record

ArticleScientific reports2025

CD55 may be a new target for colorectal cancer treatment.

Qiong Luo, Yingjia Mao, Rong Yu, Fuqian Zhao, Hongmei Niu, Daofu Shen, Huan Tian, Lei Wang

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

8 authors.

Qiong Luo *Third Ward of General Surgery, Department of Affiliated Hengyang Hospital of Hunan Normal University, Hengyang Central Hospital, Hengyang, 421001, Hunan, China.
Yingjia Mao *Medical Laboratory Center, Chifeng Municipal Hospital/Chifeng Clinical College, Inner Mongolia Medical University, Chifeng, 024000, People's Republic of China.
Rong YuMedical Laboratory Center, Chifeng Municipal Hospital/Chifeng Clinical College, Inner Mongolia Medical University, Chifeng, 024000, People's Republic of China.
Fuqian ZhaoMedical Laboratory Center, Chifeng Municipal Hospital/Chifeng Clinical College, Inner Mongolia Medical University, Chifeng, 024000, People's Republic of China.
Hongmei NiuMedical Laboratory Center, Chifeng Municipal Hospital/Chifeng Clinical College, Inner Mongolia Medical University, Chifeng, 024000, People's Republic of China.
Daofu ShenMedical Laboratory Center, Chifeng Municipal Hospital/Chifeng Clinical College, Inner Mongolia Medical University, Chifeng, 024000, People's Republic of China.
Huan TianChangsha Stomatological Hospita, Hunan Unversity of Traditional Chinese Medcine, 389th Youyi Road, Changsha, 410004, China. 1061655447@qq.com.
Lei WangMedical Laboratory Center, Chifeng Municipal Hospital/Chifeng Clinical College, Inner Mongolia Medical University, Chifeng, 024000, People's Republic of China. lncyly@126.com.

Funding

Inner Mongolia Medical University Joint Project No: YKD2022LH072Natural Science Foundation of Inner Mongolia Autonomous Region No: 2021MS08060Public Hospital Research Joint Fund Science and Technology Project No:2024GLIH0990Scientific researchproject of Hunan Provincial Health Commission No:202204010038
6 · The paper itself

Abstract

In the early stage, our research group injected lentivirus carrying blood type A antigen into tumors as a drug, and the tumor volume of mice was significantly reduced. We speculate that the complement system plays an important role in anti-tumor therapy, but the specific components are unknown. A mouse model containing blood type antibodies was established. After the mouse axilla formed tumors, lentivirus carrying different blood type antigens was used for treatment. On this basis, NK cell activity was inhibited and the complement system of the body was eliminated. Tumor formation was observed. Flow cytometry was used to observe the changes in tumor tissue and peripheral blood immune cells. Immunohistochemistry was used to observe NK cells in tumors. Proteomics was used to screen differential complement components. Transcriptomics was used to observe the gene expression differences of CT26 cells overexpressing CD55, and RT-PCR was used for verification. The changes of CEA, CA199, CA125, CA153, D-D dimer, total white blood cell count, neutrophil ratio, lymphocyte ratio, monocyte ratio, and fibrinogen in the simple colorectal cancer group, simple liver metastasis group, simple lung metastasis group, and multiple organ metastasis group were retrospectively analyzed, and ROC curves were used for evaluation; ELISA method was used to detect the changes in CD55 content in the healthy group, simple colorectal cancer group, simple liver metastasis group, simple lung metastasis group, and multiple organ metastasis group, and ROC curves were used to evaluate its clinical diagnostic ability. CCK8 and EdU methods were used to detect cell proliferation. Scratch assay and transwell assay were used to observe cell migration. Western blotting was used to observe the changes of MMP9, Vimentin and α-SMA. After the lentivirus carrying blood type A antigen was injected into the axillary tumor of mice, the tumor volume was significantly reduced compared with the control group. The proportion of NK cells in tumor tissue increased significantly. Using antibodies to block NK cell surface activation receptors and eliminate the complement system, both treatments reduced the therapeutic effect. Both blood type B and Rh blood type antigens can significantly reduce tumor volume. Eliminating complement in the body increases the incidence of liver metastasis. The proliferation degree of overexpressed CD55 in tumors is significantly increased. CD55 overexpression can significantly increase the expression of CCL2, CCL3, CCL4, CCL7, CXCL12, TLR7, CSFR1, TCAM, TNF, BTK and MMP9. CEA and CA199 are of certain value in judging liver metastasis, and CD55 has better diagnostic efficacy. Complement significantly inhibits cell proliferation. CD55 significantly promotes CT26 proliferation and migration ability. CD55 is a potential tumor promoter and diagnostic marker for colorectal cancer.

Indexed as

Colorectal NeoplasmsAnimalsCell Line, TumorFemaleHumansKiller Cells, NaturalLentivirusLiver NeoplasmsMaleMiceMice, Inbred BALB CABO blood typeCD55Colorectal cancerComplement systemTumor marker

Identifiers

PMID40596619
PMCPMC12216819

What OpenQuestion holds

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LicenceCC BY
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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.