The PI3K/AKT axis modulates AATF activity in Wilms' tumor cells
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Updated: Sep 22, 2026

Aip1p Dynamics Are Altered by the R256H Mutation in Actin
Published on: July 30, 2014
Peng Jing1,2, Jiaqiong Zou3, Kegui Weng4
1Department of Pediatric Surgery Affiliated Hospital of Northern Sichuan Medical College Nanchong China.
Abstract:
Previous studies have reported excessive expression of apoptosis-antagonizing transcription factor (AATF) in various tumors, where it reinforces the generation and development of cancers and is linked to the clinical outcome. Nevertheless, the expression and influence of AATF in Wilms' tumor (WT) is largely unknown. Here, we discovered that AATF expression was markedly increased in WT tissues as compared to the surrounding normal tissues. Elevated levels of AATF expression were related to tumor relapse and pulmonary metastasis, congruent with it being a predictor of clinical outcome in people suffering from WT. Proliferation, invasion, and migration of WT cells were suppressed by knockdown of AATF and promoted by AATF overexpression in vitro. Furthermore, the tumor generation capability of WT cells noticeably decreased after knockout of AATF in vivo. The phosphoinositide-3-kinase (PI3K)/AKT pathway modulated the activity of AATF in WT. The findings of our study indicate that AATF expression is increased in WT and can serve as a predictor of clinical outcome; in addition, it may enhance the development of WT via the PI3K/AKT axis and may be a promising marker for WT diagnosis and therapy.
Insights
Apoptosis-antagonizing transcription factor (AATF) is highly expressed in Wilms' tumor (WT), promoting cancer growth and metastasis. Targeting AATF may offer a new therapeutic strategy for WT patients.
Area of Science:
- Oncology
- Molecular Biology
- Cancer Research
Background:
- Apoptosis-antagonizing transcription factor (AATF) is overexpressed in various cancers, influencing tumor development and patient outcomes.
- The role of AATF in Wilms' tumor (WT), a common pediatric kidney cancer, remains largely uncharacterized.
Purpose of the Study:
- To investigate the expression and functional significance of AATF in Wilms' tumor.
- To explore the potential of AATF as a prognostic biomarker and therapeutic target in WT.
Main Methods:
- Quantitative analysis of AATF expression in WT tissues versus normal tissues.
- In vitro studies involving AATF knockdown and overexpression in WT cells to assess proliferation, invasion, and migration.
- In vivo xenograft models to evaluate the effect of AATF knockout on tumor formation.
- Investigation of the involvement of the phosphoinositide-3-kinase (PI3K)/AKT pathway in AATF-mediated effects.
Main Results:
- AATF expression was significantly elevated in WT tissues compared to normal tissues.
- High AATF levels correlated with increased risk of tumor relapse and pulmonary metastasis in WT patients.
- AATF knockdown inhibited WT cell proliferation, invasion, and migration in vitro.
- AATF overexpression promoted these aggressive cellular behaviors.
- AATF knockout significantly reduced tumor growth in vivo.
- The PI3K/AKT pathway was identified as a key regulator of AATF activity in WT.
Conclusions:
- AATF is upregulated in Wilms' tumor and serves as a potential predictor of poor clinical outcomes.
- AATF promotes WT development and progression through the PI3K/AKT signaling pathway.
- AATF represents a promising diagnostic marker and therapeutic target for Wilms' tumor.
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