Evidence map›Paper›PMID 39532855›Full record

ArticleCell death & disease2024

TNFAIP2 promotes HIF1α transcription and breast cancer angiogenesis by activating the Rac1-ERK-AP1 signaling axis.

Wenlong Ren, Huichun Liang, Jian Sun, Zhuo Cheng, Wenjing Liu, Yingying Wu, Yujie Shi, Zhongmei Zhou, Ceshi Chen

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 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing 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

12 citing papers in PubMed.

  1. Article
  2. [MBD1 knockdown inhibits proliferation, migration and angiogenesis of human umbilical vein endothelial cellsNan fang yi ke da xue xue bao = Journal of Southern Medical University · 2026
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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

9 authors.

Wenlong Ren *School of Life Science, University of Science & Technology of China, Hefei, Anhui, China.
Huichun Liang *Key Laboratory of Animal Models and Human Disease Mechanisms of the Chinese Academy of Sciences and Yunnan Province, Kunming Institute of Zoology, Chinese Academy of Sciences, Kunming, China.
Jian SunYunnan Key Laboratory of Breast Cancer Precision Medicine, Yunnan Cancer Hospital, The Third Affiliated Hospital of Kunming Medical University, Peking University Cancer Hospital Yunnan, Kunming, China.
Zhuo ChengKey Laboratory of Animal Models and Human Disease Mechanisms of the Chinese Academy of Sciences and Yunnan Province, Kunming Institute of Zoology, Chinese Academy of Sciences, Kunming, China.
Wenjing LiuYunnan Key Laboratory of Breast Cancer Precision Medicine, Yunnan Cancer Hospital, The Third Affiliated Hospital of Kunming Medical University, Peking University Cancer Hospital Yunnan, Kunming, China.
Yingying WuDepartment of Pathology, The First Affiliated Hospital of Kunming Medical University, Kunming, Yunnan, China.
Yujie ShiDepartment of Pathology, Henan Provincial People's Hospital, Zhengzhou University, Zhengzhou, Henan, China. shiyujie523@126.com.ORCID 0009-0005-2581-8583
Zhongmei ZhouThe School of Continuing Education, Kunming Medical University, Kunming, China. zhouzhongmei@kmmu.edu.cn.ORCID 0009-0004-2136-998X
Ceshi ChenKey Laboratory of Animal Models and Human Disease Mechanisms of the Chinese Academy of Sciences and Yunnan Province, Kunming Institute of Zoology, Chinese Academy of Sciences, Kunming, China. chenc@kmmu.edu.cn.ORCID 0000-0001-6398-3516

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Angiogenesis is well known to play a critical role in breast cancer. We previously reported that TNFAIP2 activates Rac1 to promote triple-negative breast cancer (TNBC) cell proliferation, migration, and chemoresistance. However, the potential contribution of TNFAIP2 to tumor angiogenesis remains unknown. In this study, we demonstrated that TNFAIP2 promotes TNBC angiogenesis by activating the Rac1-ERK-AP1-HIF1α signaling axis. Under hypoxia, TNFAIP2 activates Rac1 and ERK sequentially. Following that, ERK activates the AP-1 (c-Jun/Fra1) transcription factor. By employing chromatin immunoprecipitation and luciferase reporter assays, we showed that AP-1 directly interacts with the HIF1α gene promoter, thereby enhancing its transcription. The combined application of ERK inhibitors, U0126 or trametinib, with the VEGFR inhibitor Apatinib, additively suppresses angiogenesis and tumor growth of HCC1806 in nude mice. These findings provide new therapeutic strategies for TNBC.

Indexed as

Hypoxia-Inducible Factor 1, alpha SubunitMice, NudeNeovascularization, Pathologicrac1 GTP-Binding ProteinSignal TransductionTriple Negative Breast NeoplasmsAngiogenesisAnimalsCell Line, TumorCell ProliferationExtracellular Signal-Regulated MAP KinasesFemaleGene Expression Regulation, NeoplasticHumansHuman Umbilical Vein Endothelial CellsMAP Kinase Signaling SystemapatinibExtracellular Signal-Regulated MAP KinasesHIF1A protein, humanHypoxia-Inducible Factor 1, alpha SubunitNitrilesPyridinesPyridonesPyrimidinonesrac1 GTP-Binding ProteinRAC1 protein, humantrametinibTranscription Factor AP-1

Identifiers

PMID39532855
PMCPMC11557851

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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.