MORF4L2 (Mortality Factor 4 Like 2)

Qki knockdown in the adult heart leads to cardiac cachexia due to the alteration of Morf4l2 splicing. Inhibition of Morf4l2Δex3 inhibits cancer-induced cardiac cachexia, demonstrating it as a potential therapeutic target.

Components of the chromatin remodeling complex, such as ACTL6A, SMARCA1 and MORF4L2, were correlated with the "cold" tumor phenotype in both HPV-negative and HPV-positive HNSCC. This brief study highlights epigenetic chromatin factors that may drive oncogenesis and immune evasion, thereby identifying novel targets for cancer therapy in clearly defined, epigenetically-driven subtypes of HPV-negative and HPV-positive HNSCC.

GRHL2/MORF4L2/H4K12Ac/CSF1 axis plays an important role in anti-PD1 resistance. CSF1R inhibitors can reverse GRHL2/MORF4L2-mediated anti-PD1 resistance.

In the validation of clinical samples, we analyzed the expression of relevant lncRNAs in different risk groups and speculated the possible impact on the prognosis of breast cancer patients. The risk assessment tool built based on the full analysis of these mA-related genes and mA-related lncRNA libraries, as well as the mA-related lncRNAs, has a high prognostic prediction ability, which may provide a supplementary screening method for accurately judging the prognosis of BC and a new perspective for personalized treatment of breast cancer patients.

In this study, we identified an Xq22.2 microdeletion (about 24.5 kb), which contains distal enhancers of the PLP1 gene, as a likely cause of SPG2 in this family. The lack of distal enhancers may result in transcriptional repression of PLP1 in oligodendrocytes, potentially affecting its role in the maintenance of myelin, and causing SPG2 phenotype. This study has highlighted the importance of noncoding genomic alterations in the genetic etiology of SPG2.