Evidence map›Paper›PMID 39349443›Full record

ArticleCell death & disease2024

SOX4-BMI1 axis promotes non-small cell lung cancer progression and facilitates angiogenesis by suppressing ZNF24.

Ting Wen, Xiao Zhang, Yun Gao, Hong Tian, Lufeng Fan, Ping Yang

Abstract read
In one paragraph

Article in Cell death & disease, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing 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

22 citing papers in PubMed.

  1. Article
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  3. MOncogene · 2026
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  5. Article
  6. Review
  7. S3RL: Enhancing Spatial Single-Cell Transcriptomics With Separable Representation Learning.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Article
  8. Article
  9. 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

6 authors.

Ting WenDepartment of Respiratory and Critical Care Medicine, The Second Affiliated Hospital of Shandong First Medical University, Taian, Shandong, 271000, China.
Xiao ZhangDepartment of Respiratory and Critical Care Medicine, The Second Affiliated Hospital of Shandong First Medical University, Taian, Shandong, 271000, China.
Yun GaoDepartment of Internal Medicine, Shandong Provincial Taishan Hospital, Taian, Shandong, 271000, China.
Hong TianDepartment of Respiratory and Critical Care Medicine, The Second Affiliated Hospital of Shandong First Medical University, Taian, Shandong, 271000, China. mjyth@126.com.ORCID 0009-0005-3813-8608
Lufeng FanDepartment of General Surgery, Qilu Hospital (Qingdao), Cheeloo College of Medicine, Shandong University, Qingdao, Shandong, 266035, China. fanlufeng1986@126.com.
Ping YangDepartment of Oncology, Qingdao Endocrine and Diabetes Hospital & Institute, Qingdao, Shandong, 266000, China. 1306706553@qq.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The incidence of lung cancer has become the highest among all cancer types globally, also standing as a leading cause of cancer-related deaths. Lung cancer is broadly divided into small cell lung cancer (SCLC) and non-small cell lung cancer (NSCLC), with the latter accounting for 85% of total cases. SRY-box transcription factor 4 (SOX4), a crucial transcription factor, has been found to play a key role in the development of various cancers. However, the association between SOX4 and NSCLC is still unclear. This study investigated the clinical relevance of SOX4 and its potential mechanisms in the progression of NSCLC. Analysis of our NSCLC patient cohort revealed a significant increase in SOX4 levels in cancerous tissues, indicating its role as an independent prognostic indicator for NSCLC. In vitro experiments demonstrated that elevated SOX4 expression facilitated NSCLC cell migration, invasion, and EMT. Functionally, SOX4 drives NSCLC progression by enhancing the transcription and expression of B-cell-specific moloney leukemia virus insertion site 1 (BMI1). The oncogenic impact of SOX4-induced BMI1 expression on NSCLC advancement was validated through both in vivo and in vitro studies. In addition, our findings showed that BMI1 promoted the ubiquitination of histone H2A (H2Aub), leading to decreased zinc finger protein 24 (ZNF24) expression, which subsequently triggered vascular endothelial growth factor A (VEGF-A) secretion in NSCLC cells, thereby promoting NSCLC angiogenesis. Moreover, we evaluated the therapeutic potential of a BMI1 inhibitor in combination with Bevacizumab for NSCLC treatment using orthotopic models. The data presented in our study reveal a previously unrecognized role of the SOX4-BMI1 axis in promoting NSCLC progression and angiogenesis. This research significantly contributes to our knowledge of the interplay between SOX4 and BMI1 in NSCLC, potentially paving the way for the development of targeted therapies for this disease.

Indexed as

Carcinoma, Non-Small-Cell LungDisease ProgressionLung NeoplasmsNeovascularization, PathologicPolycomb Repressive Complex 1SOXC Transcription FactorsAngiogenesisAnimalsCell Line, TumorCell MovementFemaleGene Expression Regulation, NeoplasticHumansMaleMiceMice, NudeBMI1 protein, humanPolycomb Repressive Complex 1SOX4 protein, humanSOXC Transcription Factors

Identifiers

PMID39349443
PMCPMC11442842

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Registered trials

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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.