Evidence map›Paper›PMID 37644505›Full record

ArticleExperimental hematology & oncology2023

Elevated expression of the RNA-binding protein IGF2BP1 enhances the mRNA stability of INHBA to promote the invasion and migration of esophageal squamous cancer cells.

Juan-Juan Wang, Ding-Xiong Chen, Yu Zhang, Xin Xu, Yan Cai, Wen-Qiang Wei, Jia-Jie Hao, Ming-Rong Wang

Open access · goldAbstract read
In one paragraph

Article in Experimental hematology & oncology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
4.9field-weighted citation impact, top 4% of its field
1 · What the graph read from it

What it found

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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

28 citing papers in PubMed, 32 citations in OpenAlex.

  1. Article
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  4. IGF2BP1 modulates ZDHHC5-mediated NLRP3 inflammasome activation to promote mitochondrial damage and foam cell formation of vascular smooth muscle cells.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
    Article
  5. Article
  6. Review
  7. Review
  8. Article
  9. INHBA: A Protein-coding Gene Closely Related to Tumour Diseases.Current topics in medicinal chemistry · 2026
    Review
  10. Article
  11. Article
  12. Article
  13. Review
  14. The mMolecular biomedicine · 2025
    Review
  15. Review
  16. METTL3-mediated mActa biochimica et biophysica Sinica · 2025
    Article
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  18. Article
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  20. Epigenetics-targeted drugs: current paradigms and future challenges.Signal transduction and targeted therapy · 2024
    Review
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

8 authors at 2 institutions in 2 countries.

Juan-Juan WangState Key Laboratory of Molecular Oncology, Center for Cancer Precision Medicine, National Clinical Research Center for Cancer/Cancer Hospital, National Cancer Center, Chinese Academy of Medical Sciences (CAMS), Peking Union Medical College (PUMC), 17 Panjiayuan Nanli, Chaoyang District, Beijing, 100021, China.
Ding-Xiong ChenState Key Laboratory of Molecular Oncology, Center for Cancer Precision Medicine, National Clinical Research Center for Cancer/Cancer Hospital, National Cancer Center, Chinese Academy of Medical Sciences (CAMS), Peking Union Medical College (PUMC), 17 Panjiayuan Nanli, Chaoyang District, Beijing, 100021, China.
Yu ZhangState Key Laboratory of Molecular Oncology, Center for Cancer Precision Medicine, National Clinical Research Center for Cancer/Cancer Hospital, National Cancer Center, Chinese Academy of Medical Sciences (CAMS), Peking Union Medical College (PUMC), 17 Panjiayuan Nanli, Chaoyang District, Beijing, 100021, China.
Xin XuState Key Laboratory of Molecular Oncology, Center for Cancer Precision Medicine, National Clinical Research Center for Cancer/Cancer Hospital, National Cancer Center, Chinese Academy of Medical Sciences (CAMS), Peking Union Medical College (PUMC), 17 Panjiayuan Nanli, Chaoyang District, Beijing, 100021, China.
Yan CaiState Key Laboratory of Molecular Oncology, Center for Cancer Precision Medicine, National Clinical Research Center for Cancer/Cancer Hospital, National Cancer Center, Chinese Academy of Medical Sciences (CAMS), Peking Union Medical College (PUMC), 17 Panjiayuan Nanli, Chaoyang District, Beijing, 100021, China.
Wen-Qiang WeiDepartment of Cancer Epidemiology, National Clinical Research Center for Cancer/Cancer Hospital, National Cancer Center, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, 100021, China. weiwq@cicams.ac.cn.
Jia-Jie HaoState Key Laboratory of Molecular Oncology, Center for Cancer Precision Medicine, National Clinical Research Center for Cancer/Cancer Hospital, National Cancer Center, Chinese Academy of Medical Sciences (CAMS), Peking Union Medical College (PUMC), 17 Panjiayuan Nanli, Chaoyang District, Beijing, 100021, China. hjj8173@126.com.
Ming-Rong WangState Key Laboratory of Molecular Oncology, Center for Cancer Precision Medicine, National Clinical Research Center for Cancer/Cancer Hospital, National Cancer Center, Chinese Academy of Medical Sciences (CAMS), Peking Union Medical College (PUMC), 17 Panjiayuan Nanli, Chaoyang District, Beijing, 100021, China. wangmr2015@126.com.
Chinese Academy of Medical Sciences & Peking Union Medical College · CNNational Cancer Center · US

Funding

CAMS Innovation Fund for Medical Sciences CIFMS, 2021-I2M-1-018National Key Research and Development Program of China 2021YFC2501000National Natural Science Foundation of China 81930077Potential Development Projects of Cancer Hospital, CAMS PY2018B01
6 · The paper itself

Abstract

backgroundThe mechanisms underlying the occurrence and development of esophageal squamous cell carcinoma (ESCC) remains to be elucidated. The present study aims to investigate the roles and implications of IGF2BP1 overexpression in ESCC.

methodsIGF2BP1 protein expression in ESCC samples was assessed by immunohistochemistry (IHC), and the mRNA abundance of IGF2BP1 and INHBA was analyzed with TCGA datasets and by RNA in situ hybridization (RISH). The methylation level of the IGF2BP1 promoter region was detected by methylation-specific PCR (MSP-PCR). Cell viability, migration, invasion and in vivo metastasis assays were performed to explore the roles of IGF2BP1 overexpression in ESCC. RNA immunoprecipitation sequencing (RIP-seq) and mass spectrometry were applied to identify the target RNAs and interacting proteins of IGF2BP1, respectively. RIP-PCR, RNA pulldown, immunofluorescence (IF), gene-specific m

resultsIGF2BP1 overexpression was detected in ESCC tissues and associated with the depth of tumor invasion. In addition, IGF2BP1 mRNA expression in ESCC cells was negatively correlated with the level of its promoter methylation. Knockdown of IGF2BP1 inhibited ESCC cell invasion and migration as well as tumor metastasis. Mechanistically, we observed that IGF2BP1 bound and stabilized INHBA mRNA and then resulted in higher protein expression of INHBA, leading to the activation of Smad2/3 signaling, thus promoting malignant phenotypes. The mRNA level of INHBA was upregulated in ESCC tissues as well. Furthermore, IGF2BP1 interacted with G3BP stress granule assembly factor 1 (G3BP1). Knockdown of G3BP1 also down-regulated the INHBA-Smad2/3 signaling. BTYNB abolished this activated signaling and significantly attenuated the malignant phenotypes of ESCC cells.

conclusionsElevated expression of IGF2BP1 is a frequent event in ESCC tissues and might be a candidate biomarker for the disease. IGF2BP1 overexpression promotes the invasion and migration of ESCC cells by activating the INHBA-Smad2/3 pathway, providing a potential therapeutic target for ESCC patients with high expression of IGF2BP1.

Indexed as

Esophageal squamous cell carcinomaIGF2BP1INHBAInvasionMigrationRNA binding protein

Identifiers

PMID37644505
PMCPMC10466848
OpenAlexW4386255261

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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.