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- W3007216590 abstract "MAPK-activated protein kinase 2 (MK2) has diverse roles in inflammation and cancer. In this study we show that in glioblastoma cells, MK2 plays a role in the degradation of p53, the main determinant of cell fate. Importantly, we provide evidence that the MK2-dependent regulation of p53 is a common regulatory mechanism for both wild-type and mutated p53. Through the use of both pharmacological inhibitors and MK2 knockout models in glioblastoma cells with different p53 background, we show that MK2 inhibition leads to different cellular responses in response to DNA damage stimuli. In p53 wild-type cells, MK2 inhibition strongly attenuated cell proliferation. This effect was achieved through the deactivation of HDM2 ligase and this led to increased p53 wild-type expression and the transcription of senescent and apoptotic genes. MK2 inhibition increased the stability of p53 mutants, and this is key for their ability to phenotypically exhibit gain-of function properties. Thus, as a destabilizer of wild-type p53, MK2 represents a potential drug target in glioblastomas that contain p53 wild-type. However, the administration of an MK2 inhibitor in cells expressing p53 mutants may cause accelerated disease progression. These findings are highly relevant since p53 mutations occur over 50% of all cancers. Citation Format: Athena Frances Phoa, Ariadna Recasens, Lenka Munoz. MK2 inhibition stabilizes wild-type and mutated p53 in glioblastoma cells and leads to different cellular responses [abstract]. In: Proceedings of the AACR-NCI-EORTC International Conference on Molecular Targets and Cancer Therapeutics; 2019 Oct 26-30; Boston, MA. Philadelphia (PA): AACR; Mol Cancer Ther 2019;18(12 Suppl):Abstract nr A064. doi:10.1158/1535-7163.TARG-19-A064" @default.
- W3007216590 created "2020-03-06" @default.
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- W3007216590 date "2019-12-01" @default.
- W3007216590 modified "2023-09-27" @default.
- W3007216590 title "Abstract A064: MK2 inhibition stabilizes wild-type and mutated p53 in glioblastoma cells and leads to different cellular responses" @default.
- W3007216590 doi "https://doi.org/10.1158/1535-7163.targ-19-a064" @default.
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