Evidence map›Paper›PMID 41355356›Full record

ArticleCancer biology & therapy2025

Nuclear translocation of Cx43 promotes to CRC progression and associates with β-catenin accumulation.

Shuo Wang, Ziling Zhu, Yin Zhu, Jing Tan, Xiujin Shen, Huan Wen, Jian Wu, Jingyao Xu, Jiangjiang Zheng, Yuhan Chen and 2 more

Abstract read
In one paragraph

Article in Cancer biology & therapy, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed.

  1. Beyond the gap: moonlighting functions of connexins in cancer.Cell communication and signaling : CCS · 2026
    Review
  2. Review
  3. Pathology oncology research : POR · 2026
    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

12 authors.

Shuo WangHangzhou Cancer Institution, Hangzhou Cancer Hospital, Hangzhou, People's Republic of China.ORCID 0000-0002-9027-9257
Ziling ZhuZhejiang Key Laboratory for Disease Proteomics, Department of Pathology, School of Medicine, Zhejiang University, Hangzhou, People's Republic of China.
Yin ZhuDepartment of Pathology, Ningbo Yinzhou No. 2 Hospital, Ningbo, People's Republic of China.
Jing TanZhejiang Cancer Hospital, Hangzhou Institute of Medicine (HIM), Chinese Academy of Sciences, Hangzhou, People's Republic of China.
Xiujin ShenKidney Disease Center, The First Affiliated Hospital, College of Medicine, Zhejiang University; Key Laboratory of Kidney Disease Prevention and Control Technology, Hangzhou, Zhejiang Province, People's Republic of China.
Huan WenDepartment of Pathology, Hunan Provincial Hospital of Integrated Traditional Chinese and Western Medicine, Changsha, People's Republic of China.
Jian WuDepartment of Pathology, Hangzhou First People's Hospital, Hangzhou, People's Republic of China.
Jingyao XuThe Sperm Laboratory, College of Life Sciences, Zhejiang University, Hangzhou, People's Republic of China.
Jiangjiang ZhengDepartment of Pathology, Ningbo Yinzhou No. 2 Hospital, Ningbo, People's Republic of China.
Yuhan ChenThe Sperm Laboratory, College of Life Sciences, Zhejiang University, Hangzhou, People's Republic of China.
Wanxi YangThe Sperm Laboratory, College of Life Sciences, Zhejiang University, Hangzhou, People's Republic of China.
Hong DengZhejiang Key Laboratory for Disease Proteomics, Department of Pathology, School of Medicine, Zhejiang University, Hangzhou, People's Republic of China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe tumour microenvironment (TME) significantly influences intercellular communication, with several secreted factors activating both tumour cells and fibroblasts. Connexin43 (Cx43), a crucial gap junction protein, exhibits a significant regulatory role in tumourigenesis; however, the underlying regulatory mechanisms in colorectal cancer (CRC) are not fully understood.

methodsTranswell co-culture system was utilized to evaluate fibroblast-mediated effects on CRC cells. Immunohistochemical analysis was conducted on clinical specimens. Cell migration and invasion capabilities were measured using Transwell assays. Subcellular localization was assessed via immunofluorescence. Protein interactions were validated by co-immunoprecipitation.

resultsThe Wnt signalling pathway was activated in the co-culture of CRC cells and fibroblasts. Nuclear Cx43 upregulation was detected and confirmed as a pro-oncogenic factor via prognostic analysis of patient samples. Therefore, although Cx43 on the cell membrane serves as a tumour suppressor, the nuclear translocation of Cx43 has an important influence on the Wnt signalling pathway and promotes CRC progression. Nuclear translocation of Cx43 during malignant progression has a significant effect on metastasis and is regulated by secreted TGF-

conclusionWe systematically identified nuclear Cx43 as a factor promoting CRC progression. These findings highlight the novel mechanism involving the nuclear translocation of Cx43 as a promoting factor in CRC progression, and enhance our understanding of the interplay between the TME and CRC progression.

Indexed as

beta CateninCell NucleusColorectal NeoplasmsConnexin 43Cell Line, TumorCell MovementCoculture TechniquesDisease ProgressionHumansTumor MicroenvironmentWnt Signaling Pathwaybeta CateninConnexin 43CTNNB1 protein, humanGJA1 protein, humanColorectal cancerconnexin43nuclear translocationtumor microenvironmentβ-catenin

Identifiers

PMID41355356
PMCPMC12688224

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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 OpenQuestion graph.