MAF overexpression

Six compounds were selected for further experimental assay: vemurafenib, sorafenib, sildenafil, fluvastatin, erlotinib, and glimepiride. Moreover, both compounds simultaneously downregulated c-Maf protein expression to induce G1 phase arrest and apoptosis in myeloma cells. Collectively, sorafenib and glimepiride may be considered promising candidates for developing more potent c-Maf inhibitors in the future.

These results indicate that only Dis3 deficiency and the combination of c-Maf overexpression and Dis3 deficiency do not develop plasma cell neoplasm and suggest that additional oncogenic events are necessary for myelomagenesis. Further investigations are required for elucidating the mechanisms of how loss-of-function of DIS3 is involved in the development of MM.

We present new data in Sf9 cell lines suggesting that the CncC:Maf pathway plays a central role in FAW response to natural and synthetic xenobiotics. This knowledge helps to better understand detoxification gene expression and may help to design next-generation pest insect control measures.

b) Bar graph representing percentage of cycling cells. Data points are individual patients (high CTC levels, n=8; low CTC levels, n=14).

Single cell RNA sequencing and WGS of plasma cells from patients with high and low CTC levels identified a correlation between CTC levels and overrepresentation of MAF translocations in NDMM patients. This finding suggests that MAF target genes and downstream proliferation could be drivers of aggressive disease and might be used for future patient stratification.

MAFF is highly expressed in liver tumors and liver TICs, and its antisense oligo (ASO) has therapeutic potential in treating liver cancer without MAFA/MAFG gene copy number alterations (CNAs). This study reveal an additional layer for liver TIC regulation as well as circRNA function, and also provide an additional target for eliminating liver TICs, especially for liver tumor without MAFA/MAFG gene CNAs.

This method was applied to investigate metabolic changes elicited in the breast cancer cell line MCF-7 by specific inhibitors of glycolysis and electron transport chain, and by the deregulation of a specific mitochondrial enzyme (ACO2) leading to defective aerobic metabolism associated with tumor growth. In this model, mitochondrial fraction undergoes to a 13% increase upon ACO2 overexpression and the MAF function changes abruptly by altering the metabolic state of about the 25% of the mitochondrial pixels.