MELTF (Melanotransferrin)

Drug sensitivity analyses further suggested that stemness-high tumors may exhibit increased susceptibility to selected kinase inhibitors (Dasatinib, A-770041) and metabolic modulators (Phenformin, Salubrinal). OSA-associated IH is linked to stemness-associated transcriptional plasticity, immune suppression, and adverse clinical outcomes in lung cancer. The identified stemness-based gene signature provides a robust prognostic biomarker and highlights potential therapeutic vulnerabilities, supporting integrative strategies that combine stemness and immune -targeted approaches with immunotherapy in OSA-associated lung cancer.

Accordingly, Arid2 or Ss18 depletion phenocopies DMTF1 loss in reducing H3K27ac levels, expression of E2F target genes, and NSC proliferation. Thus, our study has identified DMTF1 as a potential therapeutic target to reverse the proliferation defect of aged NSC that is modeled by telomere attrition and unearthed a distinct genetic program controlled by DMTF1 in NSC.

On the other hand, it also activated iron-sulfur cluster assembly 2 (ISCA2)-mediated iron-sulfur cluster (ISC) assembly and iron starvation response to inhibit cuproptosis and ferroptosis. Collectively, our findings indicated the mechanism of the synergistic effect of ferroptosis and cuproptosis in the treatment of GC and presented a prospective therapeutic strategy through elucidating the molecular mechanism of ferroptosis and cuproptosis mediated by MTF1.

We developed and validated the ITHscore, a three-gene expression-based model with superior prognostic performance in ccRCC. The ITHscore reflects key features of aggressiveness in tumor biology, including immune evasion and ICB resistance. Its minimal gene set and consistent performance across data sets support its potential for clinical implementation in ccRCC stratification.

In vitro experiments, the combination of elesclomol (a copper ion carrier) and bortezomib (Bortezomib) demonstrated a synergistic anti-myeloma effect through excessive intracellular reactive oxygen species generation. This study provides valuable insights into the role of CRGs in MM, potentially aiding in prognosis prediction and the development of effective, personalized therapeutic strategies.

A prognostic signature composed of CDCP1, CLIC6, FURIN, KRT6A, MFI2, and P2RY13, based on PANR-DEGs, provides a theoretical framework and reference for further LUAD research.

Severe zinc depletion disrupts zinc homeostasis, downregulates p21, induces G1 cell cycle arrest, and triggers apoptosis through caspase activation, while mild depletion is well tolerated. These findings highlight the importance of zinc homeostasis in skeletal muscle cell survival and provide mechanistic insights into zinc-related muscle pathology.

We describe an innovative anticancer strategy that fully abides by the rules of chemical biology. We indeed modulate the formation of G4s in cells using ad hoc molecular tools in the aim of disturbing the homeostasis and inner functioning of lncRNAs. By exploiting cellular outcomes, we infer how this pharmacomodulation affects CRC biology and, beyond this, the fate of CRC cells owing to the flawed repertoire of correction and/or compensatory mechanisms in cancer cells.

Fluorescence images of colon cancer from different patients demonstrated a positive correlation between CDKN2A expression and the number of CD45+ immune cells. Our research has provided a comprehensive understanding of cuproptosis regulators and revealed potential prognostic biomarkers and therapeutic targets for cancers.

Using CRISPR-Cas9 to knock out ZIC2 also prevented tumor formation in nude mice. These results emphasize the critical role of MTF1 in the oncogenic process and its involvement in the ZIC2-mediated transformation associated with Cd-induced malignant changes.

We successfully developed a multi-omics prognostic model for gastric cancer that offers significant predictive value for patient outcomes.

If taVNS improves fatigue in these patients, it will be a significant gain in quality of life. The study was approved by the ethics committee (2024-368-f-S) and registered at the DRKS database (DRKS00036323).