CDKN2D (Cyclin Dependent Kinase Inhibitor 2D)

Our findings indicate that CspB effectively inhibits the proliferation of CRPC cells by reducing the activity of cell cycle proteins and cyclin-dependent kinase (CDK) complexes while upregulating the expression of P21 and P27 and inducing G1 phase cell cycle arrest. These results highlight the potential of CspB as a promising candidate for developing therapeutic agents aimed at targeting CRPC.

FTL and PTP4A2 silencing could suppress the proliferation, migration and invasion abilities of HCC cells. This study identified eight prognostic gene signatures related to FGFBP2+ NK cell in HCC, which may serve as potential therapeutic targets for HCC.

METTL7B is involved in BC development and progression. METTL7B may mediate m6A modification on ACSL3 mRNA to negatively regulate ferroptosis in BC cells, which provides a potential therapeutic target for BC via ferroptosis.

Our study confirms a 5-gene signature as a key biomarker for ICI response in NSCLC, enhancing treatment precision.

Ccne2, Cdk2, Cdk7, Anapc11, Anapc10, Cdc23, Cdc16, Anapc4, Cdc27, Stag1, Smc3, Smc1a, Nipbl, Pds5a, Pds5b, and Wapl genes, renowned for their role as cell cycle progression activators, were instead upregulated. Our work suggests that CBN regulates the expression of many genes related to the cell cycle, which are required for axonal maturation, migration, and synaptic plasticity, while not affecting the expression of genes involved in cell death or tumorigenesis.

In MCL, NSD2 mutations, especially p.E1099K and p.T1150A, are found in 10-15% of cases of MCL and are enriched in MCL patients who relapse from targeted therapies such as ibrutinib, an inhibitor of B cell signaling... The NSD2 mutation led to increased tumor cell growth but decreased apoptosis due to the dysregulation of epigenetic landscape and gene expression, suggesting an oncogenic reprogramming driven by activated NSD2 mutations in MCL.

The expression of CDKN2D was increased in ATLL patients. The results of this study could be helpful for understanding the pathogenic mechanism of these two diseases in the same signaling pathways.

NSD2 mutations, especially p.E1099K and p.T1150A, were identified in 10-15% of cases of MCL and are enriched in patients who relapse from targeted therapies such as ibrutinib... The NSD2 mutation led to increased tumor cell growth but decreased apoptosis due to the dysregulation of epigenetic landscape and transcriptome, suggesting an oncogenic reprogramming driven by an activated NSD2 mutation in MCL.

The inhibition of proliferation and migration of CC cells following transfection with sh-LINC01012 was reversed following co-transfection of sh-LINC01012 and CDKN2D short hairpin RNA. These findings suggested that upregulated LINC01012 expression in CC may stimulate the proliferation and migration of cancer cells, thus promoting CC progression via downregulation of CDKN2D.

Finally, a potential rBH3 motif was identified in mammalian and osteichthyan p19INK4d (p19, cyclin dependent kinase 4 inhibitor d). These findings demonstrate that the interaction between MCL1 and other cellular proteins mediated by the rBH3 motif may be conserved throughout jawed vertebrates.