MAGEB2 (MAGE Family Member B2)

The present study identified novel loci potentially influencing CRC susceptibility under THM exposure, highlighting the importance of integrating environmental and genetic data to better understand environmental driven cancer risks. Further research is needed to confirm these results and clarify underlying mechanisms.

Importantly, a number of X-linked Methdep CG genes (e.g., FMR1NB, GAGE2A, MAGEB2/C2, PAGE2, VCX3A/B) maintained this maternal-specific imprinting after fertilization, and were expressed exclusively in female preimplantation embryos, which inherit a paternal X chromosome. Together, our study using the CTexploreR package has allowed us to show that X-linked CG genes undergo transient maternal imprinting and contribute therefore to transcriptional sexual dimorphism in early embryos.

TSP-1 is an anti-angiogenic protein that activates TGFβ1. Restoring levels of TSP-1 or TGFβ1 results in the inability of MAGEB2 to drive proliferation, suggesting that MAGEB2-expressing tumors might be more susceptible to therapies that induce or activate TSP-1 or TGFβ1 signaling.

Some DEMs could be biomarkers or therapeutic targets for HCC. Moreover, we found that MAGEB2 was significantly elevated in HCC tissues for the first time, and its association with HCC needs to be explored by functional studies.

This study underscores the tumor-suppressive roles of MBNL1 and QKI in ESCC, proposing them as potential biomarkers and therapeutic targets for ESCC diagnosis and treatment.

The current study provides a comprehensive evaluation of CTAs, and suggests that their association with immune cells may indicate in situ immunogenic effects. The findings support the rationale to harness CTAs as targets for immunotherapy.

Furthermore, MAGEB2 was shown to be downregulated in specific NOA patients, implying that abnormal expression of MAGEB2 may impair spermatogenesis and male fertility. Our results offer new insights into the functional and regulatory mechanisms in MAGEB2-mediated human SSC line proliferation and apoptosis.

Ponicidin may be a promising agent for the treatment of GBC effectively and safely.