Evidence map›Paper›PMID 39167955›Full record

ArticleTranslational oncology2024

IGFBP1 promotes the proliferation and migration of lung adenocarcinoma cells through the PPARα pathway.

Yunyun Li, Xuelian Yang, Tao Han, Jiawei Zhou, Yafeng Liu, Jianqiang Guo, Ziqin Liu, Ying Bai, Yingru Xing, Xuansheng Ding and 2 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Translational oncology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing 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

6 citing papers in PubMed.

  1. 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

12 authors.

Yunyun LiSchool of Medicine, Anhui University of Science and Technology, Huainan, Anhui, China; Anhui Occupational Health and Safety Engineering Laboratory, Huainan, Anhui, China.
Xuelian YangSchool of Medicine, Anhui University of Science and Technology, Huainan, Anhui, China; Anhui Occupational Health and Safety Engineering Laboratory, Huainan, Anhui, China.
Tao HanSchool of Medicine, Anhui University of Science and Technology, Huainan, Anhui, China; Anhui Occupational Health and Safety Engineering Laboratory, Huainan, Anhui, China.
Jiawei ZhouSchool of Medicine, Anhui University of Science and Technology, Huainan, Anhui, China; Anhui Occupational Health and Safety Engineering Laboratory, Huainan, Anhui, China.
Yafeng LiuSchool of Medicine, Anhui University of Science and Technology, Huainan, Anhui, China; Anhui Occupational Health and Safety Engineering Laboratory, Huainan, Anhui, China.
Jianqiang GuoSchool of Medicine, Anhui University of Science and Technology, Huainan, Anhui, China; Anhui Occupational Health and Safety Engineering Laboratory, Huainan, Anhui, China.
Ziqin LiuSchool of Medicine, Anhui University of Science and Technology, Huainan, Anhui, China; Anhui Occupational Health and Safety Engineering Laboratory, Huainan, Anhui, China.
Ying BaiSchool of Medicine, Anhui University of Science and Technology, Huainan, Anhui, China; Anhui Occupational Health and Safety Engineering Laboratory, Huainan, Anhui, China; Key Laboratory of Industrial Dust Deep Reduction and Occupational Health and Safety of Anhui Higher Education Institutes, Huainan, Anhui, China.
Yingru XingDepartment of Clinical Laboratory, Anhui Zhongke Gengjiu Hospital, Hefei, China.
Xuansheng DingSchool of Medicine, Anhui University of Science and Technology, Huainan, Anhui, China; School of pharmacy, China Pharmaceutical University, Nanjing, China. Electronic address: 1020030749@cpu.edu.cn.
Jing WuSchool of Medicine, Anhui University of Science and Technology, Huainan, Anhui, China; Anhui Occupational Health and Safety Engineering Laboratory, Huainan, Anhui, China; Key Laboratory of Industrial Dust Deep Reduction and Occupational Health and Safety of Anhui Higher Education Institutes, Huainan, Anhui, China; Key Laboratory of Industrial Dust Prevention and Control & Occupational Safety and Health of the Ministry of Education, Anhui University of Science and Technology, Huainan, Anhui, China. Electronic address: wujing8008@126.com.
Dong HuSchool of Medicine, Anhui University of Science and Technology, Huainan, Anhui, China; Anhui Occupational Health and Safety Engineering Laboratory, Huainan, Anhui, China; Key Laboratory of Industrial Dust Deep Reduction and Occupational Health and Safety of Anhui Higher Education Institutes, Huainan, Anhui, China; Key Laboratory of Industrial Dust Prevention and Control & Occupational Safety and Health of the Ministry of Education, Anhui University of Science and Technology, Huainan, Anhui, China; Department of Laboratory Medicine, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, China. Electronic address: austhudong@126.com.

Funding

Evaluating Possible Auditory and Psychological Biomarkers of Sound IntoleranceI01CX002149 · VA · PORTLAND VA MEDICAL CENTER · PI THEODOROFF, SARAH · 2020 to 2023
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CSRD VA I01 CX002149
6 · The paper itself

Abstract

backgroundThe immune status is closely linked to cancer progression, metastasis, and prognosis. Lipid metabolism, crucial for reshaping immune status, plays a key role in regulating the advancement of lung adenocarcinoma (LUAD) and deserves further investigation.

methodsThis study classifies LUAD patients into different immune subtypes based on lipid metabolism-related genes and compares the clinical characteristics among these subtypes. Single-multi COX analysis screens out key genes related to prognosis, and a risk feature and prognostic model are constructed. Cell cloning, scratch, transwell, western blotting and flow cytometry cell cycle analysis to detect the function of key genes. A subcutaneous tumor animal model is used to investigate the in vivo function and molecular mechanisms of key genes.

resultsLUAD patients are classified into three immune subtypes, among which C3 subtype has lower immune status and higher frequency of gene mutations, and show lower immunoreactivity in immunotherapy. COX analysis identified a prognostic model for four lipid metabolism factors (IGFBP1, NR0B2, PPARA, and POMC). IGFBP1, a core gene in this model, is highly expressed in the C3 subtype. Functionally, knocking down IGFBP1 significantly inhibits tumor cell cloning, scratch, and migration abilities, and downregulates the expression of cell cycle and EMT-related proteins. Knocking down IGFBP1 significantly inhibits tumor burden (P < 0.05). Mechanistically, knocking down IGFBP1 inhibits the activation of PPARα to regulate tumor cell growth.

conclusionsThis study found that lipid metabolism genes are closely related to LUAD, and IGFBP1 may be a key gene in regulating tumor growth and development.

Indexed as

BioinformaticsInsulin-like growth factor binding protein 1 (IGFBP1)Lipid metabolismLUADPeroxisome proliferator-activated receptor α (PPARα)

Identifiers

PMID39167955
PMCPMC11382126

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.