Evidence map›Paper›PMID 38831470›Full record

ArticleJournal of translational medicine2024

IFI16 promotes the progression of clear cell renal cell carcinoma through the IL6/PI3K/AKT axis.

Ke Lu, Yan Zhao, Yu Li, Zhenyu Fu, Yongchang Chen, Ying Kong, Gang Li

Abstract read
In one paragraph

Article in Journal of translational medicine, 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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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.

Ke Lu *Department of Urology, The First Affiliated Hospital of Soochow University, Suzhou, 215000, Jiangsu, China.
Yan Zhao *Department of Urology, Xuzhou Cancer Hospital, Affiliated Hospital of Jiangsu University, Xuzhou, 221000, Jiangsu, China.
Yu Li *Department of Urology, The First Affiliated Hospital of Soochow University, Suzhou, 215000, Jiangsu, China.
Zhenyu FuDepartment of Urology, Affiliated Changshu Hospital of Nantong University, Changshu, 215500, Jiangsu, China.
Yongchang ChenDepartment of Urology, Affiliated Changshu Hospital of Nantong University, Changshu, 215500, Jiangsu, China. chenyc9998@163.com.
Ying KongDepartment of Urology, The First Affiliated Hospital of Soochow University, Suzhou, 215000, Jiangsu, China. kongying12@suda.edu.cn.
Gang LiDepartment of Urology, The First Affiliated Hospital of Soochow University, Suzhou, 215000, Jiangsu, China. szurol@163.com.ORCID 0009-0009-3481-644X

Funding

Suzhou "Kejiaoxingwei" Youth Science and Technology Program KJXW2023068
6 · The paper itself

Abstract

backgroundClear cell renal cell carcinoma (ccRCC) is a common disease in the urinary system, with a high incidence and poor prognosis in advanced stages. Although γ-interferon-inducible protein 16 (IFI16) has been reported to play a role in various tumors, its involvement in ccRCC remains poorly documented, and the molecular mechanisms are not yet clear.

methodsWe conducted bioinformatics analysis to study the expression of IFI16 in ccRCC using public databases. Additionally, we analyzed and validated clinical specimens that we collected. Subsequently, we explored the impact of IFI16 on ccRCC cell proliferation, migration, and invasion through in vitro and in vivo experiments. Furthermore, we predicted downstream molecules and pathways using transcriptome analysis and confirmed them through follow-up experimental validation.

resultsIFI16 was significantly upregulated in ccRCC tissue and correlated with poor patient prognosis. In vitro, IFI16 promoted ccRCC cell proliferation, migration, and invasion, while in vivo, it facilitated subcutaneous tumor growth and the formation of lung metastatic foci. Knocking down IFI16 suppressed its oncogenic function. At the molecular level, IFI16 promoted the transcription and translation of IL6, subsequently activating the PI3K/AKT signaling pathway and inducing epithelial-mesenchymal transition (EMT).

conclusionIFI16 induced EMT through the IL6/PI3K/AKT axis, promoting the progression of ccRCC.

Indexed as

Carcinoma, Renal CellCell MovementCell ProliferationDisease ProgressionEpithelial-Mesenchymal TransitionInterleukin-6Kidney NeoplasmsNuclear ProteinsPhosphatidylinositol 3-KinasesPhosphoproteinsProto-Oncogene Proteins c-aktSignal TransductionAnimalsCell Line, TumorFemaleGene Expression Regulation, NeoplasticIFI16 protein, humanInterleukin-6Nuclear ProteinsPhosphatidylinositol 3-KinasesPhosphoproteinsProto-Oncogene Proteins c-aktClear cell renal cell carcinomaEMTIFI16PI3K/AKTTumor progression

Identifiers

PMID38831470
PMCPMC11149187

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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 OpenQuestion graph.