MAFB (MAF BZIP Transcription Factor B)

Consistently, ectopic expression of IL-4 receptor α in Mafb-deficient macrophages restored M2 phenotypes comparable to those of wild-type macrophages. These data highlight the critical cell-intrinsic role of MAFB in regulating M2-like TAMs and provide the first evidence that targeting MAFB enhances ICI efficacy in CRC by reprogramming TAMs toward an anti-tumorigenic M1-like phenotype.

Flow cytometry demonstrated an alteration in the proportion of immune cells in Mtb-infected mouse lungs due to Mafb deficiency. Together, Mafb in myeloid cells is involved not only in the functional antibacterial process of macrophages but also in immune cell recruitment in the lungs, thereby contributing to host defense against Mtb infection.

These findings offer preliminary clues for future risankizumab-based combination strategies in psoriasis.

In this study, we focused on SUMOylation and investigated the importance of the SUMOylation consensus sequence in MAFK for MAFK-induced EMT, cellular migration and invasion, tumor and sphere formation, acquisition of stem-like properties, and drug resistance against doxorubicin by using the non-SUMOylation mimic mutant. Additionally, our results suggest that these findings depend on the expression of ATP-binding cassette (ABC) transporter 2 (ABCG2).

This study novelly suggests ZEB2 as a transcription factor that promotes TREM2 expression. Further investigation into the role of ZEB2 in various TREM2-associated diseases is warranted.

Finally, in vivo studies indicated that M. tuberculosis-mediated increase of MafB expression was responsible for the exacerbation of M. tuberculosis infection. Thus, our results provide a functional view of MafB as a cytokine regulator as well as novel insights into host factors involved in TB susceptibility.

These findings underscore the potential of cfDNA biomarkers to enhance BC detection and reduce the rate of unnecessary biopsies.

Correlative analyses in patient cohorts and therapeutic effects in preclinical models support the clinical relevance of this pathway. Our findings uncover a novel mechanism by which MAFB promotes ovarian cancer progression through cytoskeletal remodeling and immune suppression, connecting transcriptional regulation with epitranscriptomic modifications, and identify the MAFB-WTAP-CD55 axis as a potential therapeutic target in ovarian cancer.

This study provides the chromatin accessibility map of TAMs in HCC and reveals how distal CRE-driven transcriptional programs shape TAM states. Our findings lay the foundation for understanding the epigenetic regulation of TAM heterogeneity and nominate potential targets for TAM-directed immunotherapy in HCC.

MAFB and downstream targets of its transcriptional network are now being regarded as predictive biomarkers for certain types of tumors as well as being considered as potential therapeutic targets for cancer treatment. In this review, we summarize current knowledge on both physiological and pathological roles of MAFB and highlight the impact of its deregulation on hematological cancer initiation and progression.

Tobacco consumption significantly alters salivary protein profiles, promoting chronic inflammation, oxidative stress, and DNA repair dysregulation, all of which may contribute to oral carcinogenesis. These findings emphasize the utility of MALDI-TOF MS in detecting salivary biomarkers for early diagnosis of tobacco-related oral diseases and provide insights into the molecular pathways disrupted by tobacco use.

Low expression of miR-301a-3p may serve as a warning sign for disease progression and poor prognosis in osteosarcoma patients. miR-301a-3p may inhibit malignant behaviors of osteosarcoma cells by targeting MAFB. Future studies could explore the integration of ultrasound-targeted microbubble destruction technology to enhance the targeted delivery of miR-301a-3p mimics or MAFB inhibitors, potentially overcoming limitations in drug penetration and bioavailability observed in conventional therapies.