Evidence map›Paper›PMID 40010102›Full record

ArticleNeoplasia (New York, N.Y.)2025

Sialylated IgG-activated integrin β4-Src-Erk axis stabilizes c-Myc in a p300 lysine acetyltransferase-dependent manner to promote colorectal cancer liver metastasis.

Jing Chen, Shenghua Zhang, Xinmei Huang, Qianqian Wang, Weiyan Xu, Jing Huang, Yuming Su, Qinkun Sun, Xiaojuan Du, Baocai Xing and 1 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Neoplasia (New York, N.Y.), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing 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

10 citing papers in PubMed.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Immunoglobulin G in aging and cancer.Frontiers in immunology · 2026
    Review
  7. Article
  8. Review
  9. Article
  10. 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

11 authors.

Jing ChenHepatopancreatobiliary Surgery Department I, Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education/Beijing), Peking University Cancer Hospital & Institute, Beijing, 100142, China.
Shenghua ZhangDepartment of Immunology, School of Basic Medical Sciences, Peking University, Beijing, 100191, China; NHC Key Laboratory of Medical Immunology, Peking University, Beijing, 100191, China; Medicine Innovation Center for Fundamental Research on Major Immunology-related Diseases, Peking University, Beijing, 100191, China.
Xinmei HuangDepartment of Immunology, School of Basic Medical Sciences, Peking University, Beijing, 100191, China; NHC Key Laboratory of Medical Immunology, Peking University, Beijing, 100191, China; Medicine Innovation Center for Fundamental Research on Major Immunology-related Diseases, Peking University, Beijing, 100191, China.
Qianqian WangDepartment of Immunology, School of Basic Medical Sciences, Peking University, Beijing, 100191, China; NHC Key Laboratory of Medical Immunology, Peking University, Beijing, 100191, China; Medicine Innovation Center for Fundamental Research on Major Immunology-related Diseases, Peking University, Beijing, 100191, China.
Weiyan XuDepartment of Immunology, School of Basic Medical Sciences, Peking University, Beijing, 100191, China; NHC Key Laboratory of Medical Immunology, Peking University, Beijing, 100191, China; Medicine Innovation Center for Fundamental Research on Major Immunology-related Diseases, Peking University, Beijing, 100191, China.
Jing HuangDepartment of Immunology, School of Basic Medical Sciences, Peking University, Beijing, 100191, China; NHC Key Laboratory of Medical Immunology, Peking University, Beijing, 100191, China; Medicine Innovation Center for Fundamental Research on Major Immunology-related Diseases, Peking University, Beijing, 100191, China.
Yuming SuHepatopancreatobiliary Surgery Department I, Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education/Beijing), Peking University Cancer Hospital & Institute, Beijing, 100142, China.
Qinkun SunDepartment of Obstetrics and Gynecology, Peking University Third Hospital, Beijing, 100191, China.
Xiaojuan DuDepartment of Cell Biology, School of Basic Medical Sciences, Peking University, Beijing, 100083, China.
Baocai XingHepatopancreatobiliary Surgery Department I, Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education/Beijing), Peking University Cancer Hospital & Institute, Beijing, 100142, China. Electronic address: xingbaocai88@sina.com.
Xiaoyan QiuDepartment of Immunology, School of Basic Medical Sciences, Peking University, Beijing, 100191, China; NHC Key Laboratory of Medical Immunology, Peking University, Beijing, 100191, China; Medicine Innovation Center for Fundamental Research on Major Immunology-related Diseases, Peking University, Beijing, 100191, China. Electronic address: qiuxy@bjmu.edu.cn.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundLiver metastasis is a leading cause of colorectal cancer mortality. Therefore, the underlying mechanism and potential therapeutic target of colorectal cancer liver metastasis urge to be found. Mounting evidence indicates that cancer-derived sialylated IgG promotes tumor formation and progression. However, the role of sialylated IgG in colorectal cancer liver metastasis remains undefined. MATERIALS AND

methodsAnalysis of sialylated IgG in paired tumor tissues and adjacent normal tissues from 65 colorectal cancer patients was performed using immunohistochemical staining. Functional assays of sialylated IgG were explored in vitro and in vivo. The downstream target of sialylated IgG was investigated by performing gene-set enrichment analysis, ubiquitination assay, cycloheximide chase assay, acetylation assay and co-immunoprecipitation.

resultsHere, our investigation reveals that sialylated IgG is significantly upregulated in colorectal cancer and that the increase of IgG is positively associated with liver metastasis and poor overall survival in colorectal cancer patients. Sialylated IgG promotes colorectal cancer cell migration, invasion and liver metastasis. Notably, anti-sialylated IgG antibody effectively blocks colorectal cancer liver metastasis in mouse models. Mechanistically, sialylated IgG upregulates c-Myc protein level by decreasing c-Myc ubiquitination. Moreover, we find that p300/CBP can stabilize c-Myc by reducing c-Myc ubiquitination. Overexpression of p300/CBP protects c-Myc protein level from sialylated IgG-knockdown in a lysine acetyltransferase activity-dependent manner. Furthermore, sialylated IgG upregulates p300 protein level through integrin β4-FAK-Src-Erk signaling.

conclusionCollectively, these results indicate that a novel sialylated IgG-integrin β4-FAK-Src-Erk-p300-c-Myc signaling pathway promotes colorectal cancer liver metastasis, thus providing potential therapeutic targets for colorectal cancer liver metastasis.

Indexed as

Colorectal NeoplasmsImmunoglobulin GLiver Neoplasmsp300-CBP Transcription FactorsProto-Oncogene Proteins c-mycsrc-Family KinasesAnimalsCell Line, TumorCell MovementDisease Models, AnimalE1A-Associated p300 ProteinFemaleGene Expression Regulation, NeoplasticHumansMaleMAP Kinase Signaling SystemE1A-Associated p300 ProteinEP300 protein, humanImmunoglobulin GMYC protein, humanp300-CBP-Associated Factorp300-CBP Transcription FactorsProto-Oncogene Proteins c-mycsrc-Family Kinasesc-MycColorectal cancer liver metastasisErkp300Sialylated IgG

Identifiers

PMID40010102
PMCPMC11908626

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

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 Socratic graph.