Evidence map›Paper›PMID 40285946›Full record

ArticleBiochemical genetics2026

IBSP Promotes Clear Cell Renal Cell Carcinoma Progression Through the PI3 K/AKT Pathway.

Zhen-Hua Jin, Jun Ge, Jin-Zhuo Ning

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Article in Biochemical genetics, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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1 · What the graph read from it

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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

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3 · Its place in the literature

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0 citing papers in PubMed.

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4 · The record

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5 · Who and what money

Authors and funding

3 authors.

Zhen-Hua Jin *Department of Urology, Nantong Hospital of Traditional Chinese Medicine, Nantong, 226000, Jiangsu Province, P. R. China.
Jun Ge *Department of Nephrology, Yantai Affiliated Hospital of Binzhou Medical Univesity, Yantai, 264100, Shandong Province, P. R. China.
Jin-Zhuo NingDepartment of Urology, Renmin Hospital of Wuhan University, Wuhan, 430060, Hubei Province, P. R. China. njz120511@whu.edu.cn.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Our objective is to reveal IBSP expression within clear cell renal cell carcinoma (ccRCC) and the mechanism behind it. IBSP expression and its clinical significance in ccRCC were analyzed using the TCGA dataset. Both Western blotting and immunohistochemistry were utilized to examine IBSP expressions in clinical ccRCC specimens. Moreover, CCK-8, Annexin V-FITC/PI, wound healing, and Transwell assays were utilized to determine IBSP's role in ccRCC progression in vitro. In addition, Western blotting was deployed to ascertain levels of IBSP, PI3K/p-PI3K, and AKT/p-AKT. The TCGA database and our tissue data showcased that, unlike normal tissues, IBSP was significantly overexpressed in ccRCC tissues. Down-regulating IBSP reduces cell abilities to proliferate, migrate, and invade, besides promoting apoptosis in vitro. In vitro and in vivo, IBSP down-regulation inhibited ccRCC growth cells by suppressing PI3K/AKT phosphorylation. IBSP acts as a potential oncogene and could be a prognostic biomarker and therapeutic target for ccRCC. Furthermore, targeting IBSP may enhance existing treatment strategies, such as combining it with PI3K/AKT inhibitors to improve patient outcomes.

Indexed as

Carcinoma, Renal CellKidney NeoplasmsPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktSignal TransductionAnimalsApoptosisCell Line, TumorCell MovementCell ProliferationDisease ProgressionFemaleGene Expression Regulation, NeoplasticHumansMaleMicePhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktCcRCCIBSPPI3 K/AKT signaling

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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.