Evidence map›Paper›PMID 39910585›Full record

ArticleWorld journal of surgical oncology2025

PTEN suppresses renal cell carcinoma proliferation and migration via inhibition of the PI3K/AKT pathway.

Xu Xu, Yuan-Yue Tang, Xiaohong Liang, Wen Luo, Dong-Mei Jiang, Jie Chen

Erratum issuedAbstract read
In one paragraph

Article in World journal of surgical oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing 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

7 citing papers in PubMed.

  1. Exercise inhibits proliferation and induces apoptosis of lung adenocarcinoma cells via the POU2F2-SPOCD1-PI3K/AKT signaling axis.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors.

Xu Xu *Department of Haematology, The First Affiliated Hospital of Naval Medical University, No.168 Changhai Road, Yangpu District, Shanghai, 200433, China.
Yuan-Yue Tang *Department of Haematology, The First Affiliated Hospital of Naval Medical University, No.168 Changhai Road, Yangpu District, Shanghai, 200433, China.
Xiaohong Liang *Department of Urology, Fudan University Shanghai Cancer Center, No. 270 Dongan Road, Xuhui District, Shanghai, 200032, China.
Wen LuoDepartment of Haematology, The First Affiliated Hospital of Naval Medical University, No.168 Changhai Road, Yangpu District, Shanghai, 200433, China.
Dong-Mei JiangDepartment of Haematology, The First Affiliated Hospital of Naval Medical University, No.168 Changhai Road, Yangpu District, Shanghai, 200433, China. jiangyan.zhoufang@163.com.
Jie ChenDepartment of Haematology, The First Affiliated Hospital of Naval Medical University, No.168 Changhai Road, Yangpu District, Shanghai, 200433, China. chenjiedoctor@smmu.edu.cn.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundRenal cell carcinoma (RCC) is a frequent and aggressive type of kidney cancer with limited therapeutic options. Although phosphatase and tensin homolog (PTEN) have been recognized as a potential tumor suppressor in all kinds of cancers, its function in RCC remains to be thoroughly elucidated.

objectiveThis article was recruited to examine the PTEN's role in managing the PI3K/AKT pathway and its impact on the RCC cell proliferation and migration.

methodsThis study collected renal cancer and adjacent non-cancerous tissue samples from our hospital. HK-2 and 786-O cells were used, with 786-O cells divided into control, vector, and oe-PTEN groups. PTEN and related protein levels were detected using RT-qPCR and Western blot. Statistical analyses were performed using the Mann-Whitney U test and Kruskal-Wallis H test. Cell viability and migration were assessed using the CCK-8 assay and wound healing assay. All analyses were conducted with SPSS 22.0 software, with statistical significance defined as p < 0.05.

resultsRT-qPCR results showed that PTEN expression was significantly increased in RCC tumor tissues compared to normal tissues (p < 0.01). However, PTEN mRNA levels were significantly reduced in 786-O cells compared to HK-2 cells (p < 0.01). In 786-O cells with low PTEN expression, further induction of PTEN overexpression significantly inhibited PI3K/AKT signaling activity (p < 0.01), accompanied by decreased cell viability and migration ability. These results indicate that the expression pattern of PTEN in RCC is complex, but its overexpression can exert tumor-suppressive effects by inhibiting the PI3K/AKT signaling pathway.

conclusionOur findings demonstrate that PTEN overexpression in RCC cells leads to decreased PI3K/AKT signaling, decreasing cell viability and migration. This study highlights the critical role of PTEN in RCC progression and suggests potential therapeutic targets for intervention.

Indexed as

Carcinoma, Renal CellKidney NeoplasmsPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktPTEN PhosphohydrolaseApoptosisCell MovementCell ProliferationFemaleGene Expression Regulation, NeoplasticHumansMaleMiddle AgedPrognosisSignal TransductionTumor Cells, CulturedPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktPTEN PhosphohydrolasePTEN protein, humanCell migrationCell proliferationPI3K/AKT pathwayPTENRenal cell carcinoma

Identifiers

PMID39910585
PMCPMC11796115

What Socratic holds

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LicenceCC BY-NC-ND
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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 Socratic graph.