Evidence map›Paper›PMID 38685529›Full record

ArticleJournal of advanced research2025

KRAS/PI3K axis driven GTF3C6 expression and promotes LUAD via FAK pathway.

Xingzhao Ji, Mingqiang Liu, Tianyi Zhang, Weiying Zhang, Fuyuan Xue, Qiang Wan, Yi Liu

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of advanced research, 2025. 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
1.1field-weighted citation impact, top 23% 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

5 citing papers in PubMed, 3 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

7 authors at 1 institution in 1 country.

Xingzhao JiDepartment of Pulmonary and Critical Care Medicine, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, Shandong 250021, China; Shandong Key Laboratory of Infections Respiratory Disease, Medical Science and Technology Innovation Center, Shandong First Medical University & Shandong Academy of Medical Sciences, Jinan, Shandong, China.
Mingqiang LiuKey Laboratory of Cell Metabolism in Medical and Health of Shandong Provincial Health Commission, Central Hospital Affiliated to Shandong First Medical University, Jinan, Shandong 250021, China; Department of Pharmacy, Pingdu People's Hospital, Qingdao, Shandong 266799, China.
Tianyi ZhangKey Laboratory of Cell Metabolism in Medical and Health of Shandong Provincial Health Commission, Central Hospital Affiliated to Shandong First Medical University, Jinan, Shandong 250021, China.
Weiying ZhangDepartment of Pulmonary and Critical Care Medicine, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, Shandong 250021, China.
Fuyuan XueKey Laboratory of Cell Metabolism in Medical and Health of Shandong Provincial Health Commission, Central Hospital Affiliated to Shandong First Medical University, Jinan, Shandong 250021, China.
Qiang WanKey Laboratory of Cell Metabolism in Medical and Health of Shandong Provincial Health Commission, Central Hospital Affiliated to Shandong First Medical University, Jinan, Shandong 250021, China. Electronic address: wanqiang@sdu.edu.cn.
Yi LiuDepartment of Pulmonary and Critical Care Medicine, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, Shandong 250021, China; Shandong Key Laboratory of Infections Respiratory Disease, Medical Science and Technology Innovation Center, Shandong First Medical University & Shandong Academy of Medical Sciences, Jinan, Shandong, China. Electronic address: liuyishanyi@email.sdu.edu.cn.
Shandong Provincial Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionEffective targeting drugs for KRAS mutation-mediated Lung Adenocarcinoma (LUAD) are currently are limited.

objectivesInvestigating and intervening in the downstream key target genes of KRAS is crucial for clinically managing KRAS mutant-driven LUAD. GTF3C6, a newly identified member of the general transcription factor III (GTF3) family, plays a role in the transcription of RNA polymerase III (pol III)-dependent genes. However, its involvement in cancer remains unexplored.

methodsThis study examined the expression, roles, and potential molecular mechanisms of GTF3C6 in LUAD tissues, LSL-Kras

resultsWe present the first evidence that GTF3C6 is highly expressed in LUAD tissues, LSL-Kras

conclusionOur findings demonstrate that GTF3C6, driven by KRAS mutation, promotes LUAD development by regulating FAK phosphorylation, suggesting its potential as a biomarker and therapeutic target in KRAS mutant-driven LUAD.

Indexed as

Adenocarcinoma of LungFocal Adhesion Kinase 1Lung NeoplasmsPhosphatidylinositol 3-KinasesProto-Oncogene Proteins p21(ras)Trans-ActivatorsAnimalsCell Line, TumorCell ProliferationGene Expression Regulation, NeoplasticHumansMiceMutationSignal TransductionFocal Adhesion Kinase 1KRAS protein, humanPhosphatidylinositol 3-KinasesProto-Oncogene Proteins p21(ras)PTK2 protein, humanTrans-ActivatorsFAKGTF3C6KRASLUAD

Identifiers

PMID38685529
PMCPMC11976405
OpenAlexW4395956802

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
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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.