Loss of RNF2 delays tumour development in BAP1-deficient mesothelioma

2024 · doi:10.1101/2024.04.26.591241
preprint OA: closed CC-BY-NC-ND-4.0
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The paper investigates how the Polycomb/PR-DUB pathway changes when BAP1 is lost in malignant mesothelioma, focusing on the role of H2AK119ub1 and its dependence on the E3 ubiquitin ligase RNF2 (RING1B). Using Rnf2 knockout, the authors show that reducing H2AK119ub1 decreases clonogenic potential of Bap1-deficient mesothelioma cells in vitro and delays tumor onset in vivo. They explicitly frame a caveat that prior studies have shown variable importance of H2AK119ub1 across different cell types. This paper does not explicitly discuss endometriosis or adenomyosis; it was included in the corpus via a keyword match in the upstream search index.

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Abstract

The tumour suppressor gene BAP1 is mutated in more than half of the malignant mesothelioma patients. This catalytic subunit of Polycomb repressive deubiquitinating (PR-DUB) complex, plays an important role in maintaining gene expression levels by deubiquitinating the PRC1-mediated histone H2A lysine 119 mono-ubiquitination (H2AK119ub1). Published studies report varying degrees of importance of H2AK119ub1 in Polycomb-regulated gene expression in different cell types. Recently published data by our own lab suggests a global redistribution of the H2AK119ub1 mark from promoter to intergenic regions upon loss of BAP1. PRC1-mediated mono-ubiquitination is dependent on the E3 ubiquitin ligase function of RNF2 (RING1B). Here, by knocking-out Rnf2 , we show that loss of H2AK119ub1 levels leads to a decrease in clonogenic potential of Bap1 -deficient mesothelioma cells in vitro and a delay in tumour onset in vivo .
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Abstract The tumour suppressor gene BAP1 is mutated in more than half of the malignant mesothelioma patients. This catalytic subunit of Polycomb repressive deubiquitinating (PR-DUB) complex, plays an important role in maintaining gene expression levels by deubiquitinating the PRC1-mediated histone H2A lysine 119 mono-ubiquitination (H2AK119ub1). Published studies report varying degrees of importance of H2AK119ub1 in Polycomb-regulated gene expression in different cell types. Recently published data by our own lab suggests a global redistribution of the H2AK119ub1 mark from promoter to intergenic regions upon loss of BAP1. PRC1-mediated mono-ubiquitination is dependent on the E3 ubiquitin ligase function of RNF2 (RING1B). Here, by knocking-out Rnf2, we show that loss of H2AK119ub1 levels leads to a decrease in clonogenic potential of Bap1-deficient mesothelioma cells in vitro and a delay in tumour onset in vivo. Competing Interest Statement The authors have declared no competing interest.

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