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Research Article
The transcription factor Spalt and human homologue SALL4 induce cell invasion via the dMyc-JNK pathway in Drosophila
Jie Sun, Junzheng Zhang, Dan Wang, Jie Shen
Biology Open 2020 9: bio048850 doi: 10.1242/bio.048850 Published 24 March 2020
Jie Sun
Department of Entomology and MOA Key Laboratory for Monitory and Green Control of Crop Pest, China Agricultural University, Beijing 100193, China
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Junzheng Zhang
Department of Entomology and MOA Key Laboratory for Monitory and Green Control of Crop Pest, China Agricultural University, Beijing 100193, China
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Dan Wang
Department of Entomology and MOA Key Laboratory for Monitory and Green Control of Crop Pest, China Agricultural University, Beijing 100193, China
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  • For correspondence: shenjie@cau.edu.cn dwang@cau.edu.cn
Jie Shen
Department of Entomology and MOA Key Laboratory for Monitory and Green Control of Crop Pest, China Agricultural University, Beijing 100193, China
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  • For correspondence: shenjie@cau.edu.cn dwang@cau.edu.cn
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ABSTRACT

Cancer cell metastasis is a leading cause of mortality in cancer patients. Therefore, revealing the molecular mechanism of cancer cell invasion is of great significance for the treatment of cancer. In human patients, the hyperactivity of transcription factor Spalt-like 4 (SALL4) is sufficient to induce malignant tumorigenesis and metastasis. Here, we found that when ectopically expressing the Drosophila homologue spalt (sal) or human SALL4 in Drosophila, epithelial cells delaminated basally with penetration of the basal lamina and degradation of the extracellular matrix, which are essential properties of cell invasion. Further assay found that sal/SALL4 promoted cell invasion via dMyc-JNK signaling. Inhibition of the c-Jun N-terminal kinase (JNK) signaling pathway through suppressing matrix metalloprotease 1, or basket can achieve suppression of cell invasion. Moreover, expression of dMyc, a suppressor of JNK signaling, dramatically blocked cell invasion induced by sal/SALL4 in the wing disc. These findings reveal a conserved role of sal/SALL4 in invasive cell movement and link the crucial mediator of tumor invasion, the JNK pathway, to SALL4-mediated cancer progression.

This article has an associated First Person interview with the first author of the paper.

Footnotes

  • Competing interests

    The authors declare no competing or financial interests.

  • Author contributions

    Conceptualization: J. Shen; Methodology: J. Sun; Formal analysis: D.W., J. Sun, J. Shen; Investigation: J. Sun; Data curation: D.W., J. Sun, J.Z., J. Shen; Writing - original draft: D.W., J. Sun, J.Z.; Writing - review & editing: D.W., J. Shen; Funding acquisition: D.W., J. Shen.

  • Funding

    This research was financially supported by the Beijing Municipal Natural Science Foundation [5192010 and 6182020] and the National Natural Science Foundation of China [31872295 and 31872293].

  • Supplementary information

    Supplementary information available online at http://bio.biologists.org/lookup/doi/10.1242/bio.048850.supplemental

  • Received October 18, 2019.
  • Accepted January 22, 2020.
  • © 2020. Published by The Company of Biologists Ltd
http://creativecommons.org/licenses/by/4.0

This is an Open Access article distributed under the terms of the Creative Commons Attribution License (https://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution and reproduction in any medium provided that the original work is properly attributed.

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Keywords

  • Spalt
  • SALL4
  • JNK pathway
  • dMyc
  • Cell invasion

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Research Article
The transcription factor Spalt and human homologue SALL4 induce cell invasion via the dMyc-JNK pathway in Drosophila
Jie Sun, Junzheng Zhang, Dan Wang, Jie Shen
Biology Open 2020 9: bio048850 doi: 10.1242/bio.048850 Published 24 March 2020
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Research Article
The transcription factor Spalt and human homologue SALL4 induce cell invasion via the dMyc-JNK pathway in Drosophila
Jie Sun, Junzheng Zhang, Dan Wang, Jie Shen
Biology Open 2020 9: bio048850 doi: 10.1242/bio.048850 Published 24 March 2020

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