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CASZ1 upregulates PI3K-AKT-mTOR signaling and promotes T-cell acute lymphoblastic leukemia

Bruno A. Cardoso, Mafalda Duque, Ana Gírio, Rita Fragoso, Mariana L. Oliveira, James R. Allen, Leila R. Martins, Nádia C. Correia, André Bortolini Silveira, Alexandra Veloso, et al.
(2024) HAEMATOLOGICA. 109(6). p.1713-1725
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Abstract
CASZ1 is a conserved transcription factor involved in neural development, blood vessel assembly and heart morphogenesis. CASZ1 has been implicated in cancer, either suppressing or promoting tumor development depending on the tissue. However, the impact of CASZ1 on hematological tumors remains unknown. Here, we show that the T-cell oncogenic transcription factor TAL1 is a direct positive regulator of CASZ1, that T-cell acute lymphoblastic leukemia (T-ALL) samples at diagnosis overexpress CASZ1b isoform, and that CASZ1b expression in patient samples correlates with PI3KAKT- mTOR signaling pathway activation. In agreement, overexpression of CASZ1b in both Ba/F3 and T-ALL cells leads to the activation of PI3K signaling pathway, which is required for CASZ1b-mediated transformation of Ba/F3 cells in vitro and malignant expansion in vivo. We further demonstrate that CASZ1b cooperates with activated NOTCH1 to promote T-ALL development in zebrafish, and that CASZ1b protects human T-ALL cells from serum deprivation and treatment with chemotherapeutic drugs. Taken together, our studies indicate that CASZ1b is a TAL1-regulated gene that promotes T-ALL development and resistance to chemotherapy.
Keywords
Hematology, TUMOR-SUPPRESSOR, TAL1 COMPLEX, INHIBITION, GENE, EXPRESSION, MUTATIONS, CASTOR, PTEN, PI3K, DIFFERENTIATION

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MLA
Cardoso, Bruno A., et al. “CASZ1 Upregulates PI3K-AKT-MTOR Signaling and Promotes T-Cell Acute Lymphoblastic Leukemia.” HAEMATOLOGICA, vol. 109, no. 6, 2024, pp. 1713–25, doi:10.3324/haematol.2023.282854.
APA
Cardoso, B. A., Duque, M., Gírio, A., Fragoso, R., Oliveira, M. L., Allen, J. R., … Barata, J. T. (2024). CASZ1 upregulates PI3K-AKT-mTOR signaling and promotes T-cell acute lymphoblastic leukemia. HAEMATOLOGICA, 109(6), 1713–1725. https://doi.org/10.3324/haematol.2023.282854
Chicago author-date
Cardoso, Bruno A., Mafalda Duque, Ana Gírio, Rita Fragoso, Mariana L. Oliveira, James R. Allen, Leila R. Martins, et al. 2024. “CASZ1 Upregulates PI3K-AKT-MTOR Signaling and Promotes T-Cell Acute Lymphoblastic Leukemia.” HAEMATOLOGICA 109 (6): 1713–25. https://doi.org/10.3324/haematol.2023.282854.
Chicago author-date (all authors)
Cardoso, Bruno A., Mafalda Duque, Ana Gírio, Rita Fragoso, Mariana L. Oliveira, James R. Allen, Leila R. Martins, Nádia C. Correia, André Bortolini Silveira, Alexandra Veloso, Shunsuke Kimura, Lisa Demoen, Filip Matthijssens, Sima Jeha, Cheng Cheng, Ching-Hon Pui, Ana R. Grosso, João L. Neto, Sérgio F. De Almeida, Pieter Van Vlierberghe, Charles G. Mullighan, J. Andres Yunes, David M. Langenau, Françoise Pflumio, and João T. Barata. 2024. “CASZ1 Upregulates PI3K-AKT-MTOR Signaling and Promotes T-Cell Acute Lymphoblastic Leukemia.” HAEMATOLOGICA 109 (6): 1713–1725. doi:10.3324/haematol.2023.282854.
Vancouver
1.
Cardoso BA, Duque M, Gírio A, Fragoso R, Oliveira ML, Allen JR, et al. CASZ1 upregulates PI3K-AKT-mTOR signaling and promotes T-cell acute lymphoblastic leukemia. HAEMATOLOGICA. 2024;109(6):1713–25.
IEEE
[1]
B. A. Cardoso et al., “CASZ1 upregulates PI3K-AKT-mTOR signaling and promotes T-cell acute lymphoblastic leukemia,” HAEMATOLOGICA, vol. 109, no. 6, pp. 1713–1725, 2024.
@article{01HHCCC72MTC6RGG9V9W2ARNJG,
  abstract     = {{CASZ1 is a conserved transcription factor involved in neural development, blood vessel assembly and heart morphogenesis. CASZ1 has been implicated in cancer, either suppressing or promoting tumor development depending on the tissue. However, the impact of CASZ1 on hematological tumors remains unknown. Here, we show that the T-cell oncogenic transcription factor TAL1 is a direct positive regulator of CASZ1, that T-cell acute lymphoblastic leukemia (T-ALL) samples at diagnosis overexpress CASZ1b isoform, and that CASZ1b expression in patient samples correlates with PI3KAKT- mTOR signaling pathway activation. In agreement, overexpression of CASZ1b in both Ba/F3 and T-ALL cells leads to the activation of PI3K signaling pathway, which is required for CASZ1b-mediated transformation of Ba/F3 cells in vitro and malignant expansion in vivo. We further demonstrate that CASZ1b cooperates with activated NOTCH1 to promote T-ALL development in zebrafish, and that CASZ1b protects human T-ALL cells from serum deprivation and treatment with chemotherapeutic drugs. Taken together, our studies indicate that CASZ1b is a TAL1-regulated gene that promotes T-ALL development and resistance to chemotherapy.}},
  author       = {{Cardoso, Bruno A. and Duque, Mafalda and Gírio, Ana and Fragoso, Rita and Oliveira, Mariana L. and Allen, James R. and Martins, Leila R. and Correia, Nádia C. and Silveira, André Bortolini and Veloso, Alexandra and Kimura, Shunsuke and Demoen, Lisa and Matthijssens, Filip and Jeha, Sima and Cheng, Cheng and Pui, Ching-Hon and Grosso, Ana R. and Neto, João L. and De Almeida, Sérgio F. and Van Vlierberghe, Pieter and Mullighan, Charles G. and Yunes, J. Andres and Langenau, David M. and Pflumio, Françoise and Barata, João T.}},
  issn         = {{0390-6078}},
  journal      = {{HAEMATOLOGICA}},
  keywords     = {{Hematology,TUMOR-SUPPRESSOR,TAL1 COMPLEX,INHIBITION,GENE,EXPRESSION,MUTATIONS,CASTOR,PTEN,PI3K,DIFFERENTIATION}},
  language     = {{eng}},
  number       = {{6}},
  pages        = {{1713--1725}},
  title        = {{CASZ1 upregulates PI3K-AKT-mTOR signaling and promotes T-cell acute lymphoblastic leukemia}},
  url          = {{http://doi.org/10.3324/haematol.2023.282854}},
  volume       = {{109}},
  year         = {{2024}},
}
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