Evidence map›Paper›PMID 37636370›Full record

ArticleHeliyon2023

IL-8-mediated overexpression of ZNF274 promotes the proliferation and migration of colorectal cancer cells through the transactivation of MRPL40.

Feng Du, Yijun Zhang, Xu Ji, Nan Zhang, Junxuan Xu, Tingting Ning, Si-An Xie, Si Liu, Peng Li, Shengtao Zhu

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Heliyon, 2023. 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. Oil-Coated Nanoplastics Induce Rapid Membrane Disruption and Severe Intestinal Injury.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    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

10 authors.

Feng DuDepartment of Gastroenterology, Beijing Friendship Hospital, Capital Medical, University, National Clinical Research Centre for Digestive Disease, Beijing, Digestive Disease Centre, Beijing Key Laboratory for Precancerous Lesion of Digestive Disease, 100050 Beijing, PR China.
Yijun ZhangDepartment of Gastroenterology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College Beijing, 100730, China.
Xu JiDepartment of Gastroenterology, Beijing Friendship Hospital, Capital Medical, University, National Clinical Research Centre for Digestive Disease, Beijing, Digestive Disease Centre, Beijing Key Laboratory for Precancerous Lesion of Digestive Disease, 100050 Beijing, PR China.
Nan ZhangDepartment of Gastroenterology, Beijing Friendship Hospital, Capital Medical, University, National Clinical Research Centre for Digestive Disease, Beijing, Digestive Disease Centre, Beijing Key Laboratory for Precancerous Lesion of Digestive Disease, 100050 Beijing, PR China.
Junxuan XuDepartment of Gastroenterology, Beijing Friendship Hospital, Capital Medical, University, National Clinical Research Centre for Digestive Disease, Beijing, Digestive Disease Centre, Beijing Key Laboratory for Precancerous Lesion of Digestive Disease, 100050 Beijing, PR China.
Tingting NingDepartment of Gastroenterology, Beijing Friendship Hospital, Capital Medical, University, National Clinical Research Centre for Digestive Disease, Beijing, Digestive Disease Centre, Beijing Key Laboratory for Precancerous Lesion of Digestive Disease, 100050 Beijing, PR China.
Si-An XieDepartment of Gastroenterology, Beijing Friendship Hospital, Capital Medical, University, National Clinical Research Centre for Digestive Disease, Beijing, Digestive Disease Centre, Beijing Key Laboratory for Precancerous Lesion of Digestive Disease, 100050 Beijing, PR China.
Si LiuDepartment of Gastroenterology, Beijing Friendship Hospital, Capital Medical, University, National Clinical Research Centre for Digestive Disease, Beijing, Digestive Disease Centre, Beijing Key Laboratory for Precancerous Lesion of Digestive Disease, 100050 Beijing, PR China.
Peng LiDepartment of Gastroenterology, Beijing Friendship Hospital, Capital Medical, University, National Clinical Research Centre for Digestive Disease, Beijing, Digestive Disease Centre, Beijing Key Laboratory for Precancerous Lesion of Digestive Disease, 100050 Beijing, PR China.
Shengtao ZhuDepartment of Gastroenterology, Beijing Friendship Hospital, Capital Medical, University, National Clinical Research Centre for Digestive Disease, Beijing, Digestive Disease Centre, Beijing Key Laboratory for Precancerous Lesion of Digestive Disease, 100050 Beijing, PR China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Colorectal cancer (CRC) is one of the most prevalent malignant tumors with high morbidity and mortality rates worldwide. ZNF274, a member of the zinc-finger-protein family of transcription factors, is critical in chromosomal remodelling and tumorigenesis. However, the role of ZNF274 in CRC and the underlying molecular mechanisms remain unclear. Methods: Immunohistochemical analysis was performed to quantify the expression of ZNF274 in human CRC tissues. The Kaplan‒Meier method was used to analyse the relationship between ZNF274 expression and CRC prognosis. The correlation between ZNF274 expression and clinical features was analyzed using Cox regression analysis. Cell proliferation and migration were evaluated by CCK-8, colony formation, and Transwell assays. The limma R package was used to analyse IL-8-related differentially expressed genes in the GSE30364 dataset. The DAVID method was used to screen significantly enriched pathways. Chromatin immunoprecipitation (ChIP)-qPCR and luciferase reporter assays were performed to determine the transcriptional regulation of MRPL40 by ZNF274. Results: ZNF274 was overexpressed in CRC tissues and indicated poor prognosis. High ZNF274 expression was linked to larger tumor size, invasion, lymph node metastasis, and AJCC stage. Ectopic expression promoted CRC cell proliferation and migration. Mechanistically, MRPL40 was identified as the direct target gene that transactivates the expression of ZNF274. Moreover, IL-8 upregulated ZNF274 expression in a dose-dependent manner. Downregulation of either ZNF274 or MRPL40 expression abrogated the effect of IL-8 on promoting the proliferation and migration of CRC. Conclusion: This study revealed an oncogenic role of ZNF274 and the mechanism by which ZNF274 participated in IL-8-induced promotion of CRC progression. These findings demonstrate that ZNF274 could be used as a prognostic factor and potential therapeutic target for CRC treatment.

Indexed as

Colorectal cancerIL-8MitochondriaMRPL40Transcriptional regulationZNF274

Identifiers

PMID37636370
PMCPMC10450991

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.