Evidence map›Paper›PMID 39757674›Full record

ArticleCurrent cancer drug targets2025

Complement Factor H Promotes the Growth of Lung Adenocarcinoma Cells through the JAK2/STAT3 Signaling Pathway.

Kaili Wang, Xitan Wang, Jiang Li, Yangyang Wang, Peng Gao

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In one paragraph

Article in Current cancer drug targets, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

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3 · Its place in the literature

Who cites it

1 citing paper in PubMed.

  1. Article
4 · The record

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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

5 authors.

Kaili WangLaboratory of Thoracic Surgery, Department of Thoracic Surgery, The First Affiliated Hospital of Shandong First Medical University & Shandong Provincial Qianfoshan Hospital, Jinan, Shandong, China.
Xitan WangSchool of Clinical Medicine, Shandong Second Medical University, Weifang, Shandong, China.
Jiang LiLaboratory of Translational Medicine in Microvascular Regulation, Medical Research Center, Institute of Microvascular Medicine, Medical Research Center, The First Affiliated Hospital of Shandong First Medical University & Shandong Provincial Qianfoshan Hospital, Jinan, Shandong, China, Shandong Provincial Key Medical and Health Laboratory of Translational Medicine in Microvascular Aging, Shandong, China.
Yangyang WangLaboratory of Thoracic Surgery, Department of Thoracic Surgery, The First Affiliated Hospital of Shandong First Medical University & Shandong Provincial Qianfoshan Hospital, Jinan, Shandong, China.
Peng GaoLaboratory of Translational Medicine in Microvascular Regulation, Medical Research Center, Institute of Microvascular Medicine, Medical Research Center, The First Affiliated Hospital of Shandong First Medical University & Shandong Provincial Qianfoshan Hospital, Jinan, Shandong, China, Shandong Provincial Key Medical and Health Laboratory of Translational Medicine in Microvascular Aging, Shandong, China.ORCID 0000-0003-3321-4622

Funding

Natural Science Foundation of Shandong Province
6 · The paper itself

Abstract

backgroundOver 50% of lung adenocarcinoma patients have high levels of complement factor H (CFH) expression. Previous studies have reported that CFH inhibits the migration of endothelial cells. In this study, we investigated the mechanism by which CFH affects lung adenocarcinoma development via phosphorylation of STAT3.

methodsAdenovirus expressing mice Cfh gene was used to infect C57 mice for two weeks, and then Lewis Lung Carcinoma (LLC) was injected to develop a subcutaneous tumor. The effect of CFH on human A549 cells was also detected. Moreover, we collected CFH overexpressed conditional medium from HepG-2 cells infected with adenovirus expressing human CFH gene. A549 cells were incubated with the conditional medium, and the effect of the CFH-conditional medium on cell proliferation and migration was detected.

resultsIt was found that CFH promoted lung adenocarcinoma growth in vivo, and CFHconditional medium treatment significantly increased the viability and migration area of A549 cells. CFH-conditional medium increased the phosphorylation of JAK2 and STAT3 in A549 cells. While using STATTIC to block STAT3 phosphorylation, CFH-conditional medium treatment did not affect A549 cell viability or migration compared to the control group.

conclusionThese data suggested that CFH promoted the proliferation and migration of A549 cells by increasing the phosphorylation level of the JAK2/STAT3 signaling pathway. Furthermore, CFH has the potential to be a target for antitumor therapy.

Indexed as

Adenocarcinoma of LungComplement Factor HJanus Kinase 2Lung NeoplasmsSTAT3 Transcription FactorA549 CellsAnimalsCell MovementCell ProliferationHumansMiceMice, Inbred C57BLPhosphorylationSignal TransductionComplement Factor HJAK2 protein, humanJanus Kinase 2STAT3 protein, humanSTAT3 Transcription FactorA549 cellsCFHJAK2/STAT3.lung adenocarcinomamigrationproliferation

Identifiers

PMID39757674

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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.