ERRFI1 (ERBB Receptor Feedback Inhibitor 1)

RTK-RAS pathway alterations demonstrate strong age-, ancestry-, and treatment-specific prognostic effects and may serve as precision biomarkers of differential chemotherapy response. AI-enabled analytics substantially accelerated integrative biomarker discovery, supporting their utility for advancing precision oncology in EOCRC.

Pharmacologic inhibition of HDAC1 with panobinostat recapitulated the tumor-suppressive effects observed with MIG-6 overexpression. These findings suggest that HDAC1 may represent a potential therapeutic target in EEC and that HDAC inhibition can attenuate early tumor progression and angiogenic signaling in preclinical models. Implications: This study identifies the MIG-6/HDAC1 axis as a key regulator of angiogenesis in EEC, highlighting HDAC1 inhibition as a promising targeted therapeutic strategy for early tumor suppression.

All fusions resulted in transcriptional upregulation of USP6. In this report, we summarize the clinical, radiographic, and histologic presentations of these new cases and describe the associated fusion structures.

Furthermore, we show that miR-200c targeted the 3'UTR of ERRFI1 and reduced its expression, resulting in the resensitization of BRAFi-resistant melanoma cells to BRAFi. Our study results suggest that ERRFI1 could be a potential therapeutic target for the treatment of metastatic melanoma.

CRISPR-mediated ESR1 activation restores estrogen responsiveness in endometrial stromal cells. Combined transcriptomic, cistromic, and chromatin architecture analyses reveal ESR1's role in regulating decidualization and inflammation-related gene networks, with relevance to endometrial pathologies including endometrial cancer. This model serves as a powerful tool to study estrogen signaling in endometrial stromal cell biology and related pathologies.

Our study revealed that EGFR can accelerate the development of GDM by promoting endothelial cell dysfunction.

Also, MIG-6 overexpression promoted the epithelial-mesenchymal transition of GC cells as well as the expression of the migration-associated protein matrix metalloproteinase-9 in vitro. These results suggest that MIG-6 can serve as a new prognostic biomarker or potential therapeutic target for the identification of patients with poor survival.

We developed a robust STING pathway-related signature (STINGsig), which identified key prognostic genes and was linked to the immune microenvironment. Through in vivo experiments, we confirmed that knockdown of ERRFI1, a critical gene within the STINGsig, significantly enhances antitumor immunity and synergizes with α-PD1 therapy in a lung cancer model, underscoring its therapeutic potential in modulating immune responses.

Mechanistically, dual inhibition of XIAP and SHP2 by embelin lessens the proliferation and metastasis, activates senescence and endogenous apoptosis, inhibits cancer-related RAS/mitogen-activated protein kinase (MAPK), phosphoinositide-3-kinase (PI3K)/AKT, Janus kinase/signal transducers and activators of transcription (JAK/STAT), wingless-related integration site (Wnt), and nuclear factor kappa B (NF-κB) signaling pathways, and overcomes compensatory feedback in the MAPK signals through the modulation of mitogen-inducible gene-6 (MIG-6) and SPROUTY2 (SPRY2). Collectively, SHP2 and XIAP are potential synthetic lethal partners, and embelin warrants further development as a novel therapeutic option for alleviating KRAS-mutant NSCLC by cotargeting SHP2 and XIAP.

Our study elucidated the mechanism underlying 5-Fu-induced NAT10 downregulation, revealing that NAT10 inhibition destabilizes ERRFI1 mRNA through ac4C modifications, subsequently resulting in EGFR reactivation. A triple therapy regimen of Remodelin, cetuximab, and 5-Fu showed potential as a treatment strategy for CRC with wild-type KRAS, NRAS and BRAF.

Compared with other types of NSCLC and NPC, pLEC has distinct molecular characteristics. EBV integration, the aberrant expression of genes, as well as the loss of CNVs, may play a crucial role in the pathogenesis of pLEC. However, further research is needed to assess the potential role of the FOXD gene family as a biomarker.

The ceRNA network may provide new clues to the potential pathogenesis of KD. Finally, the new KD diagnostic model could be an effective tool for assessing the risk of KD development.