Zmat3 splices together p53-dependent tumor suppression

Kathryn T Bieging-Rolett; Laura D Attardi

doi:10.1080/23723556.2021.1898523

Zmat3 splices together p53-dependent tumor suppression

Mol Cell Oncol. 2021 Apr 29;8(3):1898523. doi: 10.1080/23723556.2021.1898523. eCollection 2021.

Authors

Kathryn T Bieging-Rolett¹, Laura D Attardi^{1

2

3}

Affiliations

¹ Division of Radiation and Cancer Biology, Department of Radiation Oncology, Stanford University School of Medicine, Stanford, CA, USA.
² Department of Genetics, Stanford University School of Medicine, Stanford, CA, USA.
³ Stanford Cancer Institute, Stanford University School of Medicine, Stanford, CA, USA.

Abstract

The tumor protein p53 (TP53, best known as p53) transcription factor is a critical tumor suppressor, but those p53-inducible genes most important for tumor suppression have remained unclear. Using unbiased RNA interference and CRISPR (Clustered Regularly Interspersed Palindromic Repeats)/Cas9 (CRISPR-associated protein 9) screens, genetically engineered mouse models, human cancer genome analysis, and integrative eCLIP-sequencing and RNA-sequencing analyses, we reveal a new branch of p53-mediated tumor suppression involving the RNA splicing regulator Zinc finger Matrin-type 3, Zmat3.

Keywords: CRISPR screen; ZMAT3; p53; splicing; tumor suppression.

Abstract

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