MYC (V-myc avian myelocytomatosis viral oncogene homolog)

HELZ2 enhances macrophage autophagy and promotes intracellular Mtb elimination by interacting with MYC and up-regulating ATG16L1. This newly identified HELZ2-MYC-ATG16L1 regulatory axis provides mechanistic insight into host defence and suggests a potential target for host-directed TB therapies.

This study delineates an epigenetic-transcriptional regulatory network that drives nodule malignancy. Our findings provide a robust theoretical foundation and a high-performance liquid biopsy tool for the precise, noninvasive diagnosis of pulmonary nodules.

In vivo, PRMT1 knockout significantly suppressed xenograft growth and reduced Ki-67 and CD31 expression. Collectively, these findings suggest that PRMT1 is an important regulator associated with cervical cancer progression and a potential candidate biomarker for prognostic assessment and therapeutic targeting, although its clinical prognostic value requires further validation.

Our work provided the most comprehensive and up-to-date view of PPIs involved in c-Myc/Max-mediated transcriptional regulation. The straightforward workflow, ease of operation, and robust performance of the m-IMAC purification make it a versatile and efficient strategy for high-throughput interactome analysis.

In conclusion, our multi-omics analysis identifies HMGA2 fusion as a promising diagnostic and prognostic biomarker for DDLPS with rhabdomyosarcomatous differentiation. The comprehensive molecular and immune landscape of this tumor subtype not only deepens our understanding of its pathophysiology but also provides critical insights for future precision medicine strategies.

The absence of MYC amplification reinforces the benign nature of these neoplasms. These findings raise new hypotheses regarding the pathogenesis of SCM and warrant further investigation into cardiac myxoid tumors.

This study confirms that 3-hydroxybenz[a]anthracene exhibits estrogen-like activity in vitro and can influence malignant biological behaviors of breast cancer cells by regulating relevant signaling pathways. These findings provide experimental evidence for further evaluating the endocrine-disrupting effects and breast cancer risks associated with such environmental pollutants.

The most common predicted interactions in PCs involve CD74 and ligands such as MIF, and we find that CD74 blockade consistently inhibits CLL cell growth in culture. Our work highlights key features of the CLL proliferative niche and provides a roadmap for identifying vulnerabilities and new therapeutic strategies.

Subsequently, we developed a mathematical model to gain insights into the disruptive role of MYC in clock regulation under disease-like conditions and, in turn, the effects of the circadian clock on MYC. We found that c-MYC oscillated in a circadian manner in U2OS cells and that the MYC protein's role is as a disruptor, but its timing can minimize its negative impact(s) on circadian rhythms.

Here, using a doxycycline-inducible OSKM mouse model, we show that prolonged systemic OSKM induction causes early lethality associated with hepatocyte dedifferentiation and oxidative stress, in the absence of tumor formation. Importantly, antioxidant treatment with N-acetylcysteine (NAC) alleviated oxidative stress and significantly improved survival without impairing reprogramming-associated cellular plasticity. These findings establish oxidative stress as a key driver of liver failure during sustained in vivo reprogramming and provide a mechanistic rationale for cyclic induction strategies.

These findings identify a PKA/PRMT5/hnRNP A1 signaling axis that promotes IRES-dependent translation and contributes to mTOR inhibitor resistance in GBM. Dual inhibition of PKA and mTOR may represent a promising therapeutic strategy.

The retention of RB1 and the presence of the NFE2L2 mutation distinguish this entity from classic SCLC, supporting a reclassification as high-grade NSCLC. Recognition of this molecular subset is vital, as NFE2L2 mutations are theoretically linked to resistance to standard platinum-based regimens, potentially necessitating therapeutic strategies distinct from standard SCLC algorithms.