Mad2 promotes Cyclin B2 recruitment to the kinetochore for guiding accurate mitotic checkpoint

Liu, Sikai; Yuan, Xiao; Gui, Ping; Liu, Ran; Durojaye, Olanrewaju Ayodeji; Hill, Donald L.; Fu, Chuanhai; Yao, Xuebiao; Dou, Zhen; Liu, Xing

doi:10.15252/embr.202154171

Cited by 7 publications

(4 citation statements)

References 67 publications

(92 reference statements)

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“…In most of the cases reported, poor checkpoint regulation due to overexpression of specific cyclins or spindle assembly factors were the cause for the appearance of mitotic slippage and subsequent tetraploidization [91,[93][94][95][96]. Our results show that RNF144B could be involved in regulating the levels of several cell cycle and spindle assembly proteins, including TPX2 [79], MAP4 [97], BCCIP [98], CCNB2 [99], RAD21 [81] and KIF4 [100].…”

Section: Discussionmentioning

confidence: 69%

The TP53-activated E3 ligase RNF144B is a tumour suppressor that prevents genomic instability

Abad,

Sandoz,

Romero

et al. 2024

J Exp Clin Cancer Res

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Background TP53, the most frequently mutated gene in human cancers, orchestrates a complex transcriptional program crucial for cancer prevention. While certain TP53-dependent genes have been extensively studied, others, like the recently identified RNF144B, remained poorly understood. This E3 ubiquitin ligase has shown potent tumor suppressor activity in murine Eμ Myc-driven lymphoma, emphasizing its significance in the TP53 network. However, little is known about its targets and its role in cancer development, requiring further exploration. In this work, we investigate RNF144B's impact on tumor suppression beyond the hematopoietic compartment in human cancers. Methods Employing TP53 wild-type cells, we generated models lacking RNF144B in both non-transformed and cancerous cells of human and mouse origin. By using proteomics, transcriptomics, and functional analysis, we assessed RNF144B's impact in cellular proliferation and transformation. Through in vitro and in vivo experiments, we explored proliferation, DNA repair, cell cycle control, mitotic progression, and treatment resistance. Findings were contrasted with clinical datasets and bioinformatics analysis. Results Our research underscores RNF144B's pivotal role as a tumor suppressor, particularly in lung adenocarcinoma. In both human and mouse oncogene-expressing cells, RNF144B deficiency heightened cellular proliferation and transformation. Proteomic and transcriptomic analysis revealed RNF144B's novel function in mediating protein degradation associated with cell cycle progression, DNA damage response and genomic stability. RNF144B deficiency induced chromosomal instability, mitotic defects, and correlated with elevated aneuploidy and worse prognosis in human tumors. Furthermore, RNF144B-deficient lung adenocarcinoma cells exhibited resistance to cell cycle inhibitors that induce chromosomal instability. Conclusions Supported by clinical data, our study suggests that RNF144B plays a pivotal role in maintaining genomic stability during tumor suppression. Graphical Abstract

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Section: Discussionmentioning

confidence: 69%

The TP53-activated E3 ligase RNF144B is a tumour suppressor that prevents genomic instability

Abad,

Sandoz,

Romero

et al. 2024

J Exp Clin Cancer Res

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“…CDK2 is a positive regulator of cell proliferation, and cell differentiation depends on its decreased activity [ 22 ]. In eukaryotic cells, CCNB1 and CCNB2 are cyclins which regulate the cell cycle and are closely related functionally [ 23 ]. Overexpression of CCB1 effectively induces cell division in post-mitotic mouse, rat and human cardiomyocytes [ 24 ].…”

Section: Discussionmentioning

confidence: 99%

Effects of µ-Conotoxin GIIIB on the cellular activity of mouse skeletal musculoblast: combined transcriptome and proteome analysis

Wu,

He,

Jia

2023

Proteome Sci

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Abstractµ-Conotoxin GIIIB (µ-CTX GIIIB) is a polypeptide containing three disulfide bridges, produced by the sea snail Conus geographus. This study was aimed to explored the cytotoxic effects of µ-CTX GIIIB on mouse skeletal musculoblast (Sol8). Sol8 cells were exposed to ouabain and veratridine to establish the cell injury model, and then treated with µ-CTX GIIIB. CCK-8 was adopted to evaluate the cytotoxicity of µ-CTX GIIIB. Then, proteomics and transcriptome were conducted, and the explore the differentially expressed genes (DEGs) and differentially expressed proteins (DEPs) affected by µ-CTX GIIIB were found. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis was used to investigate the affected signaling pathways. µ-CTX GIIIB increased the cell survival rate of injured Sol8 cells. We found and identified 1,663 DEGs and 444 DEPs influenced by µ-CTX GIIIB. 106 pairs of correlated DEGs and DEPs were selected by combining transcriptome and proteome data. The results of KEGG and GO analysis showed that µ-CTX GIIB affected the cell cycle, apoptosis, DNA damage and repair, lipid metabolism and other biological processes of Sol8 cells. µ-CTX GIIIB could affected cell cycle regulation, DNA damage repair, and activation of tumor factors, with potential carcinogenic effects. Our results provide an important basis for the study of in vitro toxicity, the mechanism of toxicity and injury prevention by µ-CTX GIIIB.

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“…The DNA was stained with 4′,6-diamidino-2-phenylindole (DAPI) from Sigma. Images were captured by DeltaVision softWoRx software (Applied Precision) and processed by deconvolution and z-stack projection ( Liu et al., 2022 ). Images were deconvolved using SoftWoRx (Applied Precision) and processed with ImageJ.…”

Section: Methodsmentioning

confidence: 99%

Sgo1 interacts with CENP-A to guide accurate chromosome segregation in mitosis

Wu,

Akbar,

Wang

et al. 2023

Journal of Molecular Cell Biology

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Shugoshin-1 (Sgo1) is necessary for maintaining sister centromere cohesion and ensuring accurate chromosome segregation during mitosis. It has been reported that the localization of Sgo1 at the centromere is dependent on Bub1-mediated phosphorylation of histone H2A at T120. However, it remains uncertain whether other centromeric proteins play a role in regulating the localization and function of Sgo1 during mitosis. Here, we show that CENP-A interacts with Sgo1 and determines the localization of Sgo1 to the centromere during mitosis. Further biochemical characterization revealed that lysine and arginine residues in the C-terminal domain of Sgo1 are critical for binding CENP-A. Interestingly, the replacement of these basic amino acids with acidic amino acids perturbed the localization of Sgo1 and Aurora B to the centromere, resulting in aberrant chromosome segregation and premature chromatid separation. Taken together, these findings reveal a previously unrecognized but direct link between Sgo1 and CENP-A in centromere plasticity control and illustrate how the Sgo1–CENP-A interaction guides accurate cell division.

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Mad2 promotes Cyclin B2 recruitment to the kinetochore for guiding accurate mitotic checkpoint

Cited by 7 publications

References 67 publications

The TP53-activated E3 ligase RNF144B is a tumour suppressor that prevents genomic instability

The TP53-activated E3 ligase RNF144B is a tumour suppressor that prevents genomic instability

Effects of µ-Conotoxin GIIIB on the cellular activity of mouse skeletal musculoblast: combined transcriptome and proteome analysis

Sgo1 interacts with CENP-A to guide accurate chromosome segregation in mitosis

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