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Abscisic acid signaling through LANCL2 and PPARγ induces activation of p38MAPK resulting in dormancy of prostate cancer metastatic cells

  • Authors:
    • Keshab Raj Parajuli
    • Younghun Jung
    • Russell S. Taichman
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    Affiliations: Department of Periodontology, University of Alabama at Birmingham School of Dentistry, Birmingham, AL 35294, USA, Department of Periodontics and Oral Medicine, University of Michigan School of Dentistry, Ann Arbor, MI 48109, USA
    Copyright: © Parajuli et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
  • Article Number: 39
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    Published online on: January 8, 2024
       https://doi.org/10.3892/or.2024.8698
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Abstract

Prostate cancer (PCa) is one the most common malignancies in men. The high incidence of bone metastasis years after primary therapy suggests that disseminated tumor cells must become dormant, but maintain their ability to proliferate in the bone marrow. Abscisic acid (ABA) is a stress response molecule best known for its regulation of seed germination, stomal opening, root shoot growth and other stress responses in plants. ABA is also synthesized by mammalian cells and has been linked to human disease. The aim of the present study was to examine the role of ABA in regulating tumor dormancy via signaling through lanthionine synthetase C‑like protein 2 (LANCL2) and peroxisome proliferator activated receptor γ (PPARγ) receptors. ABA signaling in human PCa cell lines was studied using targeted gene knockdown (KD), western blotting, quantitative PCR, cell proliferation, migration, invasion and soft agar assays, as well as co‑culture assays with bone marrow stromal cells. The data demonstrated that ABA signaling increased the expression of p21, p27 and p16, while inhibiting viability, migration, invasion and colony size in a reversable manner without toxicity. ABA also induced p38MAPK activation and NR2F1 signaling. Targeted gene KD of LANCL2 and PPARγ abrogated the cellular responses to ABA. Taken together, these data demonstrate that ABA may induce dormancy in PCa cell lines through LANCL2 and PPARγ signaling, and suggest novel targets to manage metastatic PCa growth.
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Copy and paste a formatted citation
Spandidos Publications style
Parajuli KR, Jung Y and Taichman RS: Abscisic acid signaling through LANCL2 and PPARγ induces activation of p38MAPK resulting in dormancy of prostate cancer metastatic cells. Oncol Rep 51: 39, 2024.
APA
Parajuli, K.R., Jung, Y., & Taichman, R.S. (2024). Abscisic acid signaling through LANCL2 and PPARγ induces activation of p38MAPK resulting in dormancy of prostate cancer metastatic cells. Oncology Reports, 51, 39. https://doi.org/10.3892/or.2024.8698
MLA
Parajuli, K. R., Jung, Y., Taichman, R. S."Abscisic acid signaling through LANCL2 and PPARγ induces activation of p38MAPK resulting in dormancy of prostate cancer metastatic cells". Oncology Reports 51.3 (2024): 39.
Chicago
Parajuli, K. R., Jung, Y., Taichman, R. S."Abscisic acid signaling through LANCL2 and PPARγ induces activation of p38MAPK resulting in dormancy of prostate cancer metastatic cells". Oncology Reports 51, no. 3 (2024): 39. https://doi.org/10.3892/or.2024.8698
Copy and paste a formatted citation
x
Spandidos Publications style
Parajuli KR, Jung Y and Taichman RS: Abscisic acid signaling through LANCL2 and PPARγ induces activation of p38MAPK resulting in dormancy of prostate cancer metastatic cells. Oncol Rep 51: 39, 2024.
APA
Parajuli, K.R., Jung, Y., & Taichman, R.S. (2024). Abscisic acid signaling through LANCL2 and PPARγ induces activation of p38MAPK resulting in dormancy of prostate cancer metastatic cells. Oncology Reports, 51, 39. https://doi.org/10.3892/or.2024.8698
MLA
Parajuli, K. R., Jung, Y., Taichman, R. S."Abscisic acid signaling through LANCL2 and PPARγ induces activation of p38MAPK resulting in dormancy of prostate cancer metastatic cells". Oncology Reports 51.3 (2024): 39.
Chicago
Parajuli, K. R., Jung, Y., Taichman, R. S."Abscisic acid signaling through LANCL2 and PPARγ induces activation of p38MAPK resulting in dormancy of prostate cancer metastatic cells". Oncology Reports 51, no. 3 (2024): 39. https://doi.org/10.3892/or.2024.8698
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