ArticleBMC urology2026
HSF4 promotes renal cell carcinoma progression and is associated with PI3K/Akt pathway.
Article in BMC urology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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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.
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Who cites it
1 citing paper in PubMed.
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Authors and funding
16 authors.
Funding
Abstract
backgroundRenal cell carcinoma (RCC) is a common urological malignancy, accounting for approximately 2% of global cancer-related mortality. Heat shock factors (HSFs) are transcription factors that regulate cell stress reaction. However, the exact mode of action of HSF4 in cancer, particularly RCC, is still unknown.
objectiveTo investigate the expression pattern of HSF4 in RCC and its potential molecular mechanism (especially the association with the PI3K/Akt pathway), so as to identify a new therapeutic target for RCC.
methodsBioinformatics analyses were performed to assess HSF4 expression and its prognosis relevance in RCC. The effects of HSF4 on RCC were studied with both in vitro and in vivo experiments. The transcriptome sequencing results were analyzed for both the gene knockdown and control RCC cells to predict relevant RCC signaling pathways.
resultsOur experimental results indicate that HSF4 knockdown can prevent the occurrence and spread of RCC in the body, as well as the growth and invasion of RCC cells. Mechanistically, HSF4 knockdown led to a significant decrease in the protein levels of PI3K, p-AKT, β-catenin, and c-Myc. These findings demonstrate that HSF4 promotes RCC progression by concurrently activating the PI3K/AKT and Wnt/β-catenin signaling pathways.
conclusionOur findings identify that HSF4 is highly expressed in RCC and can promote the occurrence and development of RCC. Therefore, HSF4 may be a potential therapeutic target for RCC.
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