Elevated expression levels of the protein kinase DYRK1B induce mesenchymal features in A549 lung cancer cells DOI Creative Commons

Soraya Sester,

Gerrit Wilms,

Joana Ahlburg

et al.

BMC Cancer, Journal Year: 2024, Volume and Issue: 24(1)

Published: Oct. 31, 2024

The protein kinase DYRK1B is a negative regulator of cell proliferation but has been found to be overexpressed in diverse human solid cancers. While recognized promote survival and adaption stressful conditions, the consequences elevated levels cancer cells are largely uncharted.

Language: Английский

Immunometabolism of tumor-associated macrophages: a therapeutic perspective DOI Creative Commons

A. F. Karimova,

Adelya R. Khalitova,

Роман В. Суезов

et al.

European Journal of Cancer, Journal Year: 2025, Volume and Issue: unknown, P. 115332 - 115332

Published: Feb. 1, 2025

Language: Английский

Citations

1

A safe haven for cancer cells: tumor plus stroma control by DYRK1B DOI Creative Commons

Miriam Ems,

Anna Brichkina, Matthias Lauth

et al.

Oncogene, Journal Year: 2025, Volume and Issue: unknown

Published: Jan. 25, 2025

Abstract The development of resistance remains one the biggest challenges in clinical cancer patient care and it comprises all treatment modalities from chemotherapy to targeted or immune therapy. In solid malignancies, drug is result adaptive processes occurring cells surrounding tumor microenvironment (TME). Future therapy attempts will therefore benefit targeting both, stroma compartments targets which affect both sides be highly appreciated. this review, we describe a seemingly paradoxical oncogenic mediator with potential: dual-specificity tyrosine-phosphorylation regulated kinase 1B (DYRK1B). DYRK1B promotes proliferative quiescence yet overexpressed amplified many hyperproliferative malignancies including ovarian pancreatic cancer. particular latter disease paradigmatic example for therapy-recalcitrant stroma-rich entity. Here, recent evidence suggests that exerts its features by installing protective niche directly affecting but also TME. Specifically, not only fosters cell-intrinsic like cell survival, chemoresistance, recurrence, upregulates TME cell-protective innate checkpoints down-modulates anti-tumoral macrophage functionality. article, outline well-established cell-autonomous roles extend importance control stroma. summary, appears as single novel key player creating safe haven acting cell-intrinsically and—extrinsically, leading promotion relapse. Thus, an attractive target future therapeutic approaches.

Language: Английский

Citations

0

CRISPR/Cas9-Mediated Knockout of DYRK1B in Triple Negative Breast Cancer Cells: Implications for Cell Proliferation, Apoptosis, and Therapeutic Sensitivity DOI

Asrin Rashidi,

Ernst‐Martin Füchtbauer, Zakaria Vahabzadeh

et al.

Biochemical Engineering Journal, Journal Year: 2024, Volume and Issue: unknown, P. 109553 - 109553

Published: Oct. 1, 2024

Language: Английский

Citations

0

Elevated expression levels of the protein kinase DYRK1B induce mesenchymal features in A549 lung cancer cells DOI Creative Commons

Soraya Sester,

Gerrit Wilms,

Joana Ahlburg

et al.

BMC Cancer, Journal Year: 2024, Volume and Issue: 24(1)

Published: Oct. 31, 2024

The protein kinase DYRK1B is a negative regulator of cell proliferation but has been found to be overexpressed in diverse human solid cancers. While recognized promote survival and adaption stressful conditions, the consequences elevated levels cancer cells are largely uncharted.

Language: Английский

Citations

0