Evidence map›Paper›PMID 39068456›Full record

ArticleCancer cell international2024

TGFBI promotes proliferation and epithelial-mesenchymal transition in renal cell carcinoma through PI3K/AKT/mTOR/HIF-1α pathway.

Shanzhi Zhan, Xiaojie Bai, Yiqiao Zhao, Kuerban Tuoheti, Zuhaer Yisha, Yingtong Zuo, Peixiang Lu, Tongzu Liu

Abstract read
In one paragraph

Article in Cancer cell international, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing 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

12 citing papers in PubMed.

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  12. [MIS18BP1 regulates epithelial-mesenchymal transition, proliferation, and migration of renal cancer cellsNan fang yi ke da xue xue bao = Journal of Southern Medical University
    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

8 authors.

Shanzhi Zhan *Department of Urology, Zhongnan Hospital of Wuhan University, 169 Donghu Road, Wuhan, 430071, China.
Xiaojie Bai *Department of Urology, Zhongnan Hospital of Wuhan University, 169 Donghu Road, Wuhan, 430071, China.
Yiqiao Zhao *Department of Urology, Zhongnan Hospital of Wuhan University, 169 Donghu Road, Wuhan, 430071, China.
Kuerban TuohetiDepartment of Urology, Zhongnan Hospital of Wuhan University, 169 Donghu Road, Wuhan, 430071, China.
Zuhaer YishaDepartment of Urology, Zhongnan Hospital of Wuhan University, 169 Donghu Road, Wuhan, 430071, China.
Yingtong ZuoDepartment of Urology, Zhongnan Hospital of Wuhan University, 169 Donghu Road, Wuhan, 430071, China.
Peixiang LuDepartment of Urology, Zhongnan Hospital of Wuhan University, 169 Donghu Road, Wuhan, 430071, China.
Tongzu LiuDepartment of Urology, Zhongnan Hospital of Wuhan University, 169 Donghu Road, Wuhan, 430071, China. liutongzu@163.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundRenal cell carcinoma (RCC) is presently recognized as the most prevalent kidney tumor. However, the role and underlying mechanism of action of the conversion factor-inducible protein (TGFBI), an extracellular matrix protein, in RCC remain poorly understood.

methodsIn this study, we employed Western blot, quantitative real-time polymerase chain reaction (qRT-PCR), and immunohistochemistry techniques to assess the expression of TGFBI in RCC tissues or cells. Furthermore, we analyzed the proliferation and migration of RCC cells using CCK8, cloning, scratching, and migration assays. Additionally, we examined apoptosis and cell cycle progression through flow cytometry, analysis. Lastly, we employed gene set enrichment analysis (GSEA) to investigate the biological processes associated with TGFBI, which were subsequently validated.

resultsThe findings indicate that TGFBI exhibits significantly elevated expression levels in both renal cell carcinoma (RCC) tissues and cells. Furthermore, the knockdown of TGFBI in SiRNA transfected cells resulted in the inhibition of RCC cell proliferation, migration, invasiveness, apoptosis, and alteration of the cell cycle. Additionally, TGFBI was found to impede the epithelial-mesenchymal transition (EMT) process in RCC cells. Bioinformatics analysis suggests that TGFBI may exert its influence on various biological processes in RCC through the tumor immune microenvironment. Moreover, our study demonstrates that TGFBI promotes RCC progression by activating the PI3K/AKT/mTOR/HIF-1α.

conclusionsOur research indicates that TGFBI exhibits high expression in RCC and facilitate RCC progression and metastasis through various molecular mechanisms. Hence, TGFBI has the potential to be a novel therapeutic target for the diagnosis and treatment of RCC in the future.

Indexed as

Epithelial–mesenchymal transitionInvasionMigrationPI3K/AKT/mTOR/HIF-1α pathwayRenal cell carcinomaTGFBI

Identifiers

PMID39068456
PMCPMC11282683

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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.