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Updated: Feb 8, 2026

The Encapsulation of Cell-free Transcription and Translation Machinery in Vesicles for the Construction of Cellular Mimics
Published on: October 21, 2013
A new baby in the c-Myc-directed transcriptional machinery: Che-1/AATF
Valentina Folgiero1, Cristina Sorino2, Franco Locatelli1,3
1a Department of Pediatric Hematology/Oncology and of Cell and Gene Therapy , Bambino Gesù Children's Hospital, IRCCS , Rome , Italy.
Insights
High expression of Che-1/AATF and c-Myc in pediatric B-cell precursor acute lymphoblastic leukemia (BCP-ALL) drives cancer cell proliferation. Silencing Che-1/AATF enhances chemotherapy response, identifying it as a potential therapeutic target.
Area of Science:
- Oncology
- Molecular Biology
- Pediatric Hematology
Background:
- B-cell precursor acute lymphoblastic leukemia (BCP-ALL) is the most common childhood cancer.
- While cure rates are high, novel therapeutic targets are needed.
- High expression of c-Myc and Che-1/AATF is observed in pediatric BCP-ALL.
Purpose of the Study:
- To investigate the role of c-Myc and Che-1/AATF co-expression in pediatric BCP-ALL.
- To explore Che-1/AATF as a potential therapeutic target in BCP-ALL.
Main Methods:
- Analysis of c-Myc and Che-1/AATF expression in pediatric BCP-ALL patient samples.
- Investigating the molecular mechanisms of c-Myc and Che-1/AATF co-expression.
- Assessing the effect of Che-1/AATF silencing on BCP-ALL cell proliferation and chemotherapy response.
Main Results:
- Che-1/AATF expression is crucial for c-Myc-driven blast-cell proliferation in BCP-ALL.
- High expression of c-Myc and Che-1/AATF diminishes upon remission.
- Silencing Che-1/AATF in primary BCP-ALL cells enhances sensitivity to chemotherapy.
Conclusions:
- Che-1/AATF plays a critical role in c-Myc-driven tumorigenicity in BCP-ALL.
- Che-1/AATF represents a promising novel therapeutic target for BCP-ALL treatment.
- Targeting Che-1/AATF may improve treatment outcomes for pediatric BCP-ALL patients.
Abstract:
B-cell precursor acute lymphoblastic leukemia (BCP-ALL) is the most common malignancy in childhood. Despite the high cure-rate, identifying new druggable molecular targets is still of great interest. In a cohort of BCP-ALL pediatric patients, irrespectively of the molecule/karyotype lesions found, we recently observed high expression of c-Myc and Che-1/AATF, which disappears at time of remission. Study of the molecular mechanisms involved in this co-expression revealed that Che-1 expression was crucial for induction of blast-cell proliferation driven by c-Myc. Furthermore, Che-1/AATF silencing in primary BCP-ALL cell lines improves responsiveness to chemotherapy. These data individuate Che-1 as a possible novel target in the treatment of BCP-ALL able to affect c-Myc-driven tumorigenicity.
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