Evidence map›Paper›PMID 41444594›Full record

ArticleEuropean journal of medical research2025

GAB2 regulates lipid metabolism by activating the MEK/ERK/c-Myc pathway: impact on renal cell carcinoma progression.

Weiqun Zhang, Xianming Fei, Pinqiong Qin, Yan Sun, Zhiying Zhu, Nan Huang, Xiaoying Li, Zhipeng Li, Ting Liu

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in European journal of medical research, 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

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

1 citing paper in PubMed.

  1. Article
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

9 authors.

Weiqun Zhang *Department of Clinical Laboratory, The First People's Hosiptal of Lin'an District, Hangzhou, 311300, Zhejiang, China.
Xianming Fei *Laboratory Medicine Center, Department of Clinical Laboratory, Zhejiang Provincial People's Hospital (Affliated People's Hospital), Hangzhou Medical College, Hangzhou, 310014, Zhejiang, China.
Pinqiong QinDepartment of Clinical Laboratory, The First People's Hosiptal of Lin'an District, Hangzhou, 311300, Zhejiang, China.
Yan SunDepartment of Clinical Laboratory, The First People's Hosiptal of Lin'an District, Hangzhou, 311300, Zhejiang, China.
Zhiying ZhuDepartment of Clinical Laboratory, The First People's Hosiptal of Lin'an District, Hangzhou, 311300, Zhejiang, China.
Nan HuangDepartment of Clinical Laboratory, The First People's Hosiptal of Lin'an District, Hangzhou, 311300, Zhejiang, China.
Xiaoying LiDepartment of Clinical Laboratory, The First People's Hosiptal of Lin'an District, Hangzhou, 311300, Zhejiang, China.
Zhipeng LiDepartment of Clinical Laboratory, The First People's Hosiptal of Lin'an District, Hangzhou, 311300, Zhejiang, China.
Ting LiuDepartment of Clinical Laboratory, The First People's Hosiptal of Lin'an District, Hangzhou, 311300, Zhejiang, China. 15158191568@163.com.

Funding

the Project of Zhejiang Provincial Health Department 2023KY1023
6 · The paper itself

Abstract

backgroundGrb2-associated binding protein 2 (GAB2) is a scaffold protein in the cytoplasm involved in the progression of various cancers, but its significance in renal cell carcinoma (RCC) development remains unclear. The investigation sought to explore the mechanisms of GAB2 in RCC.

methodsGAB2 mRNA levels were examined in normal renal tubular epithelial cells (HKC) and RCC cell lines (ACHN and OS-RC-2). GAB2 was knocked down or overexpressed in RCC cells, and changes in cell proliferation, apoptosis, migration, and lipid metabolism were assessed. Moreover, p-MEK, p-ERK, and c-Myc levels were measured. The MEK inhibitor U0126 was introduced to validate the underlying mechanisms. Nude mice were subcutaneously injected with ACHN cells transfected with either oe-NC or oe-GAB2 , and then treated with U0126. The MEK/ERK/c-Myc pathway, tumor growth, and lipid metabolism were subsequently evaluated.

resultsGAB2 expression was notably elevated in RCC cells compared to HKC. GAB2 knockdown markedly reduced RCC cell viability, induced apoptosis, and inhibited cell migration and lipid accumulation, whereas overexpression of GAB2 had the opposite effects. Notably, the MEK/ERK/c-Myc pathway in RCC cells was inhibited by GAB2 knockdown and activated by its overexpression. U0126 treatment altered the effects of GAB2 overexpression in RCC cells. In RCC mice, GAB2 overexpression upregulated MEK/ERK/c-Myc pathway, which was suppressed by U0126. Moreover, GAB2 overexpression promoted tumor growth and lipid synthesis in RCC mice, and U0126 counteracted these changes.

conclusionGAB2 enhances lipid accumulation by activating MEK/ERK/c-Myc pathway, thereby promoting RCC progression. GAB2 is a potential target for RCC management.

Indexed as

Adaptor Proteins, Signal TransducingCarcinoma, Renal CellKidney NeoplasmsLipid MetabolismMAP Kinase Signaling SystemProto-Oncogene Proteins c-mycAnimalsApoptosisCell Line, TumorCell MovementCell ProliferationDisease ProgressionGene Expression Regulation, NeoplasticHumansMiceMice, NudeAdaptor Proteins, Signal TransducingGAB2 protein, humanMYC protein, humanProto-Oncogene Proteins c-mycGAB2Lipid metabolismMEK/ERK/c-Myc pathwayRenal cell carcinomaTumor development

Identifiers

PMID41444594
PMCPMC12849598

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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.