Evidence map›Paper›PMID 38775031›Full record

ArticleJournal of cellular and molecular medicine2024

Chondroitin polymerizing factor promotes development and progression of colorectal cancer via facilitating transcription of VEGFB.

Yuan Huang, Zhen Zhang, Hanxing Tong, Wenzheng Qin, Quanlin Li, Lili Ma, Zhong Ren, Weifeng Chen, Yiqun Zhang, Yunshi Zhong and 2 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of cellular and molecular medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Article
  2. 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.

Yuan HuangShanghai Collaborative Innovation Center of Endoscopy, Endoscopy Center and Endoscopy Research Institute, Zhongshan Hospital, Fudan University, Shanghai, China.
Zhen ZhangShanghai Collaborative Innovation Center of Endoscopy, Endoscopy Center and Endoscopy Research Institute, Zhongshan Hospital, Fudan University, Shanghai, China.
Hanxing TongDepartment of General Surgery, Zhongshan Hospital, Fudan University, Shanghai, China.
Wenzheng QinShanghai Collaborative Innovation Center of Endoscopy, Endoscopy Center and Endoscopy Research Institute, Zhongshan Hospital, Fudan University, Shanghai, China.
Quanlin LiShanghai Collaborative Innovation Center of Endoscopy, Endoscopy Center and Endoscopy Research Institute, Zhongshan Hospital, Fudan University, Shanghai, China.
Lili MaShanghai Collaborative Innovation Center of Endoscopy, Endoscopy Center and Endoscopy Research Institute, Zhongshan Hospital, Fudan University, Shanghai, China.
Zhong RenShanghai Collaborative Innovation Center of Endoscopy, Endoscopy Center and Endoscopy Research Institute, Zhongshan Hospital, Fudan University, Shanghai, China.
Weifeng ChenShanghai Collaborative Innovation Center of Endoscopy, Endoscopy Center and Endoscopy Research Institute, Zhongshan Hospital, Fudan University, Shanghai, China.
Yiqun ZhangShanghai Collaborative Innovation Center of Endoscopy, Endoscopy Center and Endoscopy Research Institute, Zhongshan Hospital, Fudan University, Shanghai, China.
Yunshi ZhongShanghai Collaborative Innovation Center of Endoscopy, Endoscopy Center and Endoscopy Research Institute, Zhongshan Hospital, Fudan University, Shanghai, China.ORCID 0000-0001-8382-3747
Liqing YaoShanghai Collaborative Innovation Center of Endoscopy, Endoscopy Center and Endoscopy Research Institute, Zhongshan Hospital, Fudan University, Shanghai, China.
Pinghong ZhouShanghai Collaborative Innovation Center of Endoscopy, Endoscopy Center and Endoscopy Research Institute, Zhongshan Hospital, Fudan University, Shanghai, China.ORCID 0000-0002-5434-0540

Funding

Shanghai Engineering and Research Center of Diagnostic and Therapeutic Endoscopy 16DZ2280900Shanghai Engineering and Research Center of Diagnostic and Therapeutic Endoscopy 19DZ2280100
6 · The paper itself

Abstract

Colorectal cancer (CRC) is a highly prevalent malignancy affecting the digestive system on a global scale. This study aimed to explore the previously unexplored role of CHPF in the progression of CRC. Our results revealed a significant upregulation of CHPF expression in CRC tumour tissues compared to normal tissues, with its levels correlating with tumour malignancy. In vitro experiments using CRC cell lines demonstrated that inhibiting CHPF expression suppressed cell proliferation, colony formation and cell migration, while promoting apoptosis. Conversely, overexpressing CHPF had the opposite effect. Additionally, our xenograft models in mice confirmed the inhibitory impact of CHPF knockdown on CRC progression using various cell models. Mechanistic investigations unveiled that CHPF may enhance VEGFB expression through E2F1-mediated transcription. Functionally, suppressing VEGFB expression successfully mitigated the oncogenic effects induced by CHPF overexpression. Collectively, these findings suggest that CHPF may act as a tumour promoter in CRC, operating in a VEGFB-dependent manner and could be a potential target for therapeutic interventions in CRC treatment.

Indexed as

ApoptosisCell MovementCell ProliferationColorectal NeoplasmsDisease ProgressionGene Expression Regulation, NeoplasticVascular Endothelial Growth Factor BAgedAnimalsCell Line, TumorFemaleHumansMaleMiceMice, NudeN-Acetylgalactosaminyltransferaseschondroitin synthaseN-AcetylgalactosaminyltransferasesVascular Endothelial Growth Factor BVEGFB protein, humanCHPFcolorectal cancermolecular mechanismtumour promotorVEGFB

Identifiers

PMID38775031
PMCPMC11109815

What OpenQuestion 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 OpenQuestion graph.