This preprint is under consideration at Journal of Cancer Research and Clinical Oncology. A preprint is a preliminary version of a manuscript that has not completed peer review at a journal. Research Square does not conduct peer review prior to posting preprints. The posting of a preprint on this server should not be interpreted as an endorsement of its validity or suitability for dissemination as established information or for guiding clinical practice.
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Research Article
Christine Stürken
endorf: Universitatsklinikum Hamburg-Eppendorf
Corresponding Author
ORCiD: https://orcid.org/0000-0003-3997-3304
License:
This work is licensed under a CC BY 4.0 License. Read Full License
Purpose:
The transcription factor Fra-2 affects the invasive potential of breast cancer cells by dysregulating adhesion molecules in vitro. Previous results suggested that it upregulates the expression of E- and P-selectin ligands. Such selectin ligands are important members of the leukocyte adhesion cascade, which govern the adhesion and transmigration of cancer cells into the stroma of the host organ of metastasis. As so far, no in vivo data are available, this study was designed to elucidate the role of Fra-2 expression in a spontaneous breast cancer metastasis xenograft model.
Methods:
The effect of Fra-2 overexpression in two stable Fra-2 overexpressing clones of the human breast cancer cell line MDA MB231 on survival and metastatic load was studied after subcutaneous injection into scid and E- and P-selectin deficient scid mice.
Results:
Fra-2 overexpression lead to a significantly shorter overall survival and a higher amount of spontaneous lung metastases not only in scid mice, but also in E- and P-deficient mice, indicating that it regulates not only selectin ligands, but also selectin-independent adhesion processes.
Conclusion:
Thus, Fra-2 expression influences the metastatic potential of breast cancer cells by changing the expression of adhesion molecules, resulting in increased adherence to endothelial cells in a breast cancer xenograft model.
Keywords
Breast Cancer, Transcription factor, AP-1, Fra-2, Metastasis
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Peer Review Timeline
CURRENT STATUS: Under Revision
Version 1
Posted 15 Jun, 2021
No community comments so far
Editorial decision: Minor revisions needed
On 07 Jul, 2021
Reviews received
Received 20 Jun, 2021
Reviewers invited
Invitations sent on 18 Jun, 2021
Editor assigned
On 03 Jun, 2021
First submitted
On 03 Jun, 2021
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This preprint is under consideration at Journal of Cancer Research and Clinical Oncology. A preprint is a preliminary version of a manuscript that has not completed peer review at a journal. Research Square does not conduct peer review prior to posting preprints. The posting of a preprint on this server should not be interpreted as an endorsement of its validity or suitability for dissemination as established information or for guiding clinical practice.
Learn more about In Review
Research Article
Christine Stürken
endorf: Universitatsklinikum Hamburg-Eppendorf
Corresponding Author
ORCiD: https://orcid.org/0000-0003-3997-3304
Badges
Prescreen
This manuscript passed our Prescreen assessment
Complete author information
Appropriate declaration statements
Potential risks to human health
Prescreen
Peer Review Timeline
CURRENT STATUS: Under Revision
Version 1
Posted 15 Jun, 2021
No community comments so far
Editorial decision: Minor revisions needed
On 07 Jul, 2021
Reviews received
Received 20 Jun, 2021
Reviewers invited
Invitations sent on 18 Jun, 2021
Editor assigned
On 03 Jun, 2021
First submitted
On 03 Jun, 2021
Metrics
Comments: 0
PDF Downloads: ...
HTML Views: ...
License:
This work is licensed under a CC BY 4.0 License. Read Full License
Purpose:
The transcription factor Fra-2 affects the invasive potential of breast cancer cells by dysregulating adhesion molecules in vitro. Previous results suggested that it upregulates the expression of E- and P-selectin ligands. Such selectin ligands are important members of the leukocyte adhesion cascade, which govern the adhesion and transmigration of cancer cells into the stroma of the host organ of metastasis. As so far, no in vivo data are available, this study was designed to elucidate the role of Fra-2 expression in a spontaneous breast cancer metastasis xenograft model.
Methods:
The effect of Fra-2 overexpression in two stable Fra-2 overexpressing clones of the human breast cancer cell line MDA MB231 on survival and metastatic load was studied after subcutaneous injection into scid and E- and P-selectin deficient scid mice.
Results:
Fra-2 overexpression lead to a significantly shorter overall survival and a higher amount of spontaneous lung metastases not only in scid mice, but also in E- and P-deficient mice, indicating that it regulates not only selectin ligands, but also selectin-independent adhesion processes.
Conclusion:
Thus, Fra-2 expression influences the metastatic potential of breast cancer cells by changing the expression of adhesion molecules, resulting in increased adherence to endothelial cells in a breast cancer xenograft model.
Figure 1
Figure 2
Figure 3
Figure 4
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