ArticleCell death discovery2026
HSP90AA1 restrains clear cell renal cell carcinoma progression by promoting CADM1 expression and suppressing the PI3K-AKT pathway through interaction with FBXO7.
Article in Cell death discovery, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Integrated experimental and network pharmacology analyses reveal inhibitory effects of albiflorin on renal cell carcinoma cells.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Elucidating targets and mechanisms of dietary mycotoxin carcinogenesis via network toxicology, pan-cancer analysis, and molecular simulation.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- KIF7 promotes the proliferation of clear cell renal cell carcinoma by activating the WNT/β-catenin signaling pathway.Clinical and experimental medicine · 2026Article
- RGS19 drives tumor progression and immunosuppression in clear cell renal cell carcinoma by modulating CAMs and EMT.World journal of surgical oncology · 2026Article
Corrections and comments
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Authors and funding
6 authors.
Funding
Abstract
Recent studies have shown that heat shock protein 90 alpha family class A member 1 (HSP90AA1) interacts with various tumor-associated proteins, regulates their biological activity and stability, and plays an important role in various tumors. However, the role of HSP90AA1 in clear cell renal cell carcinoma (ccRCC) remains unclear. In the study, GEO and TCGA-KIRC databases were used to analyze the expression pattern and clinical significance of HSP90AA1 in ccRCC; immunohistochemistry and Western blot were used to validate HSP90AA1 expression in ccRCC tissues and cell lines; colony formation assays, EdU and TUNEL methods, cell migration and invasion experiments, and a mouse renal orthotopic xenograft tumor model were used to detect the effects of HSP90AA1 overexpression on the biological function of ccRCC; Co-IP and RNA-seq experiments were utilized to explore the downstream regulatory mechanism of HSP90AA1. Our results showed that HSP90AA1 expression was significantly downregulated in ccRCC, and its reduced expression was associated with tumor metastasis. HSP90AA1 overexpression markedly inhibited the proliferation and metastasis ability of ccRCC cells. HSP90AA1 bound to F-box only protein 7 (FBXO7) and accelerated its protein expression. FBXO7 was expressed at low level in ccRCC, and its decreased expression was closely related to unfavorable pathological features of tumors and poor patient prognosis. FBXO7 overexpression promoted cell adhesion molecule 1 (CADM1) expression and suppressed the PI3K-AKT signaling pathway. Knocking down FBXO7 expression on the basis of HSP90AA1 overexpression significantly reversed the cell phenotype inhibition caused by HSP90AA1 overexpression, downregulated CADM1 expression, and activated the PI3K-AKT signaling pathway. In summary, HSP90AA1 exhibited a low expression pattern in ccRCC, and HSP90AA1 overexpression promoted CADM1 expression and inhibited the PI3K-AKT pathway, thereby suppressing the proliferation and metastasis of ccRCC.
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Registered trials
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