Evidence map›Paper›PMID 37580771›Full record

ArticleCell communication and signaling : CCS2023

PECAM-1 drives β-catenin-mediated EndMT via internalization in colon cancer with diabetes mellitus.

Qing Wu, Xingxing Du, Jianing Cheng, Xiuying Qi, Huan Liu, Xiaohong Lv, Xieyang Gong, Changxin Shao, Muhong Wang, Luxiao Yue and 5 more

Open access · goldAbstract readVideo-Audio Media
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell communication and signaling : CCS, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed, 1 pooled it
3.0field-weighted citation impact, top 8% 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

10 citing papers in PubMed, 1 synthesis or guideline pooled it, 13 citations in OpenAlex.

  1. Pooled it
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  6. Review
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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

15 authors at 1 institution in 1 country.

Qing Wu *Department of Anatomy, Harbin Medical University, Harbin, China.
Xingxing Du *Department of Anatomy, Harbin Medical University, Harbin, China.
Jianing Cheng *Department of Anatomy, Harbin Medical University, Harbin, China.
Xiuying QiDepartment of Anatomy, Harbin Medical University, Harbin, China.
Huan LiuDepartment of Humanities Foundation, Heilongjiang Nursing College, Harbin, China.
Xiaohong LvDepartment of Anatomy, Harbin Medical University, Harbin, China.
Xieyang GongDepartment of Obstetrics and Gynecology, the Second Affiliated Hospital of Harbin Medical University, Harbin, China.
Changxin ShaoDepartment of Obstetrics and Gynecology, the Second Affiliated Hospital of Harbin Medical University, Harbin, China.
Muhong WangColorectal Cancer Surgical Ward 2, Harbin Medical University Cancer Hospital, Harbin, China.
Luxiao YueDepartment of Anatomy, Harbin Medical University, Harbin, China.
Xin YangDepartment of Anatomy, Harbin Medical University, Harbin, China.
Shiyu LiDepartment of Anatomy, Harbin Medical University, Harbin, China.
Yafang ZhangDepartment of Anatomy, Harbin Medical University, Harbin, China. yafangzhang2008@aliyun.com.
Xuemei LiDepartment of Anatomy, Harbin Medical University, Harbin, China. xuemeili@hrbmu.edu.cn.
Huike YangDepartment of Anatomy, Harbin Medical University, Harbin, China. huikeyang@hrbmu.edu.cn.ORCID http://orcid.org/0000-0003-3876-4914
Harbin Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundDiabetes mellitus (DM) is considered to be a risk factor in carcinogenesis and progression, although the biological mechanisms are not well understood. Here we demonstrate that platelet-endothelial cell adhesion molecule 1 (PECAM-1) internalization drives β-catenin-mediated endothelial-mesenchymal transition (EndMT) to link DM to cancer.

methodsThe tumor microenvironment (TME) was investigated for differences between colon cancer with and without DM by mRNA-microarray analysis. The effect of DM on colon cancer was determined in clinical patients and animal models. Furthermore, EndMT, PECAM-1 and Akt/GSK-3β/β-catenin signaling were analyzed under high glucose (HG) and human colon cancer cell (HCCC) supernatant (SN) or coculture conditions by western and immunofluorescence tests.

resultsDM promoted the progression and EndMT occurrence of colon cancer (CC). Regarding the mechanism, DM induced PECAM-1 defection from the cytomembrane, internalization and subsequent accumulation around the cell nucleus in endothelial cells, which promoted β-catenin entry into the nucleus, leading to EndMT occurrence in CC with DM. Additionally, Akt/GSK-3β signaling was enhanced to inhibit the degradation of β-catenin, which regulates the process of EndMT.

conclusionsPECAM-1 defects and/or internalization are key events for β-catenin-mediated EndMT, which is significantly boosted by enhanced Akt/GSK-3β signaling in the DM-associated TME. This contributes to the mechanism by which DM promotes the carcinogenesis and progression of CC. Video Abstract.

Indexed as

beta CateninColonic NeoplasmsDiabetes MellitusPlatelet Endothelial Cell Adhesion Molecule-1AnimalsEndothelial CellsGlycogen Synthase Kinase 3 betaHumansProto-Oncogene Proteins c-aktTumor Microenvironmentbeta CateninCTNNB1 protein, humanGlycogen Synthase Kinase 3 betaPECAM1 protein, humanPlatelet Endothelial Cell Adhesion Molecule-1Proto-Oncogene Proteins c-aktColon cancerDiabetes mellitusEndMTPECAM-1β-catenin

Identifiers

PMID37580771
PMCPMC10426208
OpenAlexW4385806696

What Socratic holds

Textmetadata
LicenceCC BY
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.