Evidence map›Paper›PMID 38664392›Full record

ArticleCell death & disease2024

TMEM9 promotes lung adenocarcinoma progression via activating the MEK/ERK/STAT3 pathway to induce VEGF expression.

Zhiqian Wang, Peng Zhao, Kaihua Tian, Zhongshi Qiao, Hao Dong, Jie Li, Zitong Guan, Hui Su, Yang Song, Xuezhen Ma

Open access · goldAbstract 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 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
5.9field-weighted citation impact, top 3% of its field
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

16 citing papers in PubMed, 14 citations in OpenAlex.

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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

10 authors at 2 institutions in 1 country.

Zhiqian WangDepartment of Oncology, Medical College of Qingdao University, Qingdao, Shandong, China.ORCID 0009-0001-8413-4537
Peng ZhaoBiotherapy Center, Qingdao Central Hospital, University of Health and Rehabilitation Sciences, Qingdao, Shandong, China.
Kaihua TianDepartment of Thoracic Surgery, The Affiliated Hospital of Qingdao University, Qingdao, Shandong, China.
Zhongshi QiaoDepartment of Oncology, Medical College of Qingdao University, Qingdao, Shandong, China.
Hao DongDepartment of Oncology, Medical College of Qingdao University, Qingdao, Shandong, China.
Jie LiDepartment of Oncology, Medical College of Qingdao University, Qingdao, Shandong, China.
Zitong GuanDepartment of Oncology, Medical College of Qingdao University, Qingdao, Shandong, China.
Hui SuDepartment of Oncology, LiaochengPeople's Hospital, Liaocheng, Shandong, China.
Yang SongDepartment of Nutrition and Food Hygiene, School of Public Health, Medical College of Qingdao University, Qingdao, Shandong, China. qdsongyang@126.com.
Xuezhen MaDepartment of Oncology, Qingdao Central Hospital, University of Health and Rehabilitation Sciences, Affiliated Qingdao Central Hospital of Qingdao University, Qingdao, Shandong, China. 18660229289@126.com.ORCID 0009-0001-9368-5138
Qingdao University · CNLiaocheng People's Hospital · CN

Funding

National Natural Science Foundation of China (National Science Foundation of China) 82072927Natural Science Foundation of Shandong Province (Shandong Provincial Natural Science Foundation) No.ZR2022MH301
6 · The paper itself

Abstract

Abnormal Transmembrane protein 9 (TMEM9) expression has been identified in various human tumors. However, the prognostic potential and mechanistic role of TMEM9 in lung adenocarcinoma (LUAD) remain unclear. Here, we first found a significant upregulation of TMEM9 in LUAD tissues, and TMEM9 expression was positively correlated with microvessel density (MVD), T stage, and clinical stage. Survival analysis demonstrated TMEM9 was an independent indicator of poor prognosis in LUAD patients. In addition, downregulation of TMEM9 suppressed tumor growth and metastasis in vitro and in vivo models, and reduced HUVEC proliferation, migration, and tube formation in a cancer cell/HUVEC coculture model. Furthermore, TMEM9 upregulated VEGF expression, and VEGF-neutralizing antibodies reversed HUVEC angiogenesis and cancer cell migration ability caused by overexpression of TMEM9. In contrast, recombinant VEGF (rVEGF) abolished the inhibitory effect of TMEM9-knockdown LUAD cells on HUVEC angiogenesis and tumor cell migration. Moreover, we showed that TMEM9 upregulated VEGF expression by activating the mitogen-activated protein kinase/extracellular signal-regulated kinase/STAT3 (MEK/ERK/STAT3) pathway. Together, our study provides mechanistic insights into the role of TMEM9 in LUAD and highlights the potential of targeting the TMEM9/MEK/ERK/STAT3/VEGF pathway as a novel therapy for preventing LUAD progression.

Indexed as

Adenocarcinoma of LungDisease ProgressionLung NeoplasmsMAP Kinase Signaling SystemMembrane ProteinsSTAT3 Transcription FactorVascular Endothelial Growth Factor AA549 CellsAnimalsCell Line, TumorCell MovementCell ProliferationFemaleGene Expression Regulation, NeoplasticHumansHuman Umbilical Vein Endothelial CellsMembrane ProteinsSTAT3 protein, humanSTAT3 Transcription FactorTMEM9 protein, humanVascular Endothelial Growth Factor AVEGFA protein, human

Identifiers

PMID38664392
PMCPMC11045738
OpenAlexW4395449587

What Socratic holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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 Socratic graph.