Evidence map›Paper›PMID 38802900›Full record

ArticleJournal of translational medicine2024

Ferredoxin 1: a gatekeeper in halting lung adenocarcinoma progression through activation of the GPRIN2 signaling pathway.

Ming Liu, Shaoxian Wu, Haoyu Wu, You Zhou, Xinyu Zhang, Dawei Zhu, Jingting Jiang

Abstract read
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Article in Journal of translational medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing 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

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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

5 citing papers in PubMed.

  1. Role of Ferredoxin 1Cancer pathogenesis and therapy · 2026
    Review
  2. Article
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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

7 authors.

Ming LiuDepartment of Tumor Biological Diagnosis and Treatment Center, The Third Affiliated Hospital of Soochow University, Changzhou, 213003, Jiangsu, China.
Shaoxian WuDepartment of Tumor Biological Diagnosis and Treatment Center, The Third Affiliated Hospital of Soochow University, Changzhou, 213003, Jiangsu, China.
Haoyu WuDepartment of Tumor Biological Diagnosis and Treatment Center, The Third Affiliated Hospital of Soochow University, Changzhou, 213003, Jiangsu, China.
You ZhouDepartment of Tumor Biological Diagnosis and Treatment Center, The Third Affiliated Hospital of Soochow University, Changzhou, 213003, Jiangsu, China.
Xinyu ZhangDepartment of Respiratory and Critical Care Medicine, The Affiliated Changzhou No.2 People's Hospital of Nanjing Medical University, Changzhou, China.
Dawei ZhuDepartment of Tumor Biological Diagnosis and Treatment Center, The Third Affiliated Hospital of Soochow University, Changzhou, 213003, Jiangsu, China. zhudawei@suda.edu.cn.
Jingting JiangDepartment of Tumor Biological Diagnosis and Treatment Center, The Third Affiliated Hospital of Soochow University, Changzhou, 213003, Jiangsu, China. jiangjingting@suda.edu.cn.ORCID 0000-0002-3128-9762

Funding

Changzhou Clinical Medical Center and Outstanding Talent of Changzhou "The 14th Five-Year Plan" High-Level Health Talents Training Project 2022CZBJ056Grant from Changzhou Medical Center of Nanjing Medical University CZKYCMCC202202Jiangsu Provincial Key Research and Development Program BE2022719National Natural Science Foundation of China 32270955Natural Science Foundation of Jiangsu Province BK20211065Science and Technology Project of Changzhou Health Commission ZD202337
6 · The paper itself

Abstract

backgroundLung adenocarcinoma (LUAD) is a highly lethal form of lung cancer. Despite advancements in treatments, managing LUAD is still challenging due to its aggressive behavior. Recent studies indicate that various molecular pathways, including the dysregulation of ferredoxin 1 (FDX1), play roles in LUAD progression. FDX1, a crucial protein in cellular redox reactions and energy metabolism, has been linked to several cancers. However, its exact role in the development of LUAD is not yet fully understood.

methodsWe investigated the role of ferredoxin 1 (FDX1) in LUAD progression through analysis of its expression in LUAD tissues and its impact on patient survival. Functional assays were performed to assess the effects of FDX1 overexpression on LUAD cell proliferation, migration, and invasion. A xenograft model was employed to evaluate the tumorigenesis potential of LUAD cells with FDX1 overexpression. Mechanistic insights into FDX1 regulation were gained through depletion experiments targeting the G protein-regulated inducer of neurite outgrowth 2 (GPRIN2)/PI3K signaling pathway.

resultsFDX1 expression was down-regulated in LUAD tissues, correlating with shorter patient survival. Overexpression of FDX1 suppressed LUAD cell proliferation, migration, and invasion in vitro, and inhibited tumorigenesis in vivo. Mechanistically, the GPRIN2/PI3K signaling pathway was implicated in FDX1 regulation, as depletion of GPRIN2 reversed the effects of FDX1 overexpression on cellular functions.

conclusionsOur findings highlight FDX1 as a potential tumor suppressor in LUAD, acting through modulation of the GPRIN2/PI3K signaling pathway. These results suggest FDX1 as a promising therapeutic target for LUAD treatment, warranting further investigation into its clinical relevance.

Indexed as

Adenocarcinoma of LungCell MovementCell ProliferationDisease ProgressionLung NeoplasmsReceptors, G-Protein-CoupledSignal TransductionAnimalsCarcinogenesisCell Line, TumorFemaleFerredoxinsGene Expression Regulation, NeoplasticHumansMaleMiceFDX1 protein, humanFerredoxinsPhosphatidylinositol 3-KinasesReceptors, G-Protein-CoupledCuproptosisFDX1GPRIN2Lung adenocarcinoma

Identifiers

PMID38802900
PMCPMC11131317

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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.