A safe haven for cancer cells: tumor plus stroma control by DYRK1B
Miriam Ems1, Anna Brichkina2, Matthias Lauth3
1Department of Gastroenterology, Endocrinology and Metabolism, Center for Tumor and Immune Biology, Philipps University Marburg, Marburg, Germany.
Oncogene
|January 25, 2025
Summary
Dual-specificity tyrosine-phosphorylation regulated kinase 1B (DYRK1B) drives cancer resistance by protecting tumor cells and the tumor microenvironment (TME). Targeting DYRK1B offers a novel therapeutic strategy for overcoming treatment resistance in solid malignancies.
Area of Science:
- Oncology
- Molecular Biology
- Cancer Therapeutics
Background:
- Drug resistance is a major challenge in cancer care, impacting all treatment modalities.
- Resistance arises from adaptive processes in cancer cells and the tumor microenvironment (TME).
- Targeting both tumor and stromal compartments is crucial for future cancer therapies.
Purpose of the Study:
- To review the role of dual-specificity tyrosine-phosphorylation regulated kinase 1B (DYRK1B) as an oncogenic mediator.
- To highlight DYRK1B's potential in overcoming cancer drug resistance.
- To explore DYRK1B's impact on both cancer cells and the TME.
Main Methods:
- Literature review of DYRK1B's function in solid malignancies.
- Analysis of DYRK1B's cell-autonomous and TME-related oncogenic activities.
- Examination of DYRK1B's role in immune checkpoint regulation and macrophage function.
Main Results:
- DYRK1B is overexpressed in hyperproliferative malignancies like ovarian and pancreatic cancers.
- DYRK1B promotes cancer cell survival, chemoresistance, and disease recurrence.
- DYRK1B modulates the TME by upregulating immune checkpoints and down-regulating anti-tumoral macrophages.
Conclusions:
- DYRK1B acts as a key mediator creating a protective niche for cancer cells.
- DYRK1B influences both intrinsic cancer cell processes and extrinsic TME functions.
- DYRK1B represents an attractive therapeutic target for enhancing cancer treatment efficacy.
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