YBX1 (Y-Box Binding Protein 1)

Consequently, SNHG18 deficiency fosters an immunosuppressive TME and promotes PCa BM. SNHG18 expression may serve as a predictive biomarker for ICB response, offering a novel strategy to overcome immunotherapy resistance in PCa BM.

TAFA4 acts as a neuron-derived mediator of neuroimmune crosstalk in IVDD that modulates macrophage polarization and oxidative stress, thereby delaying disc degeneration. This neuron-immune axis represents a potential therapeutic target.

Clinically, analysis of a small set of CRC specimens suggests elevated YBX1 lactylation, consistent with its potential pathological relevance. Together, these results uncover a lactylation-dependent mechanism that governs m5C RNA recognition and contributes to YBX1's oncogenic activity.

Moreover, SOX4 overexpression enhanced ATP production and the levels of mitochondrial respiratory chain complexs while reducing ROS and mtROS levels in CD4+T cells, with no significant change in mitochondrial mass. Conclusion We demonstrate that SOX4 induces a plastic Treg-like state in CD4+T cells, modulates the expression of key molecules associated with Treg suppressive function, and enhances their oxidative phosphorylation.

These findings suggest that DNMT1/3B-skewed methylation at the SOX9/DEFA5 promoters may be counteracted by ten-eleven translocation-mediated counter-demethylation. Collectively, our data indicate that afatinib modulates Paneth-like differentiation markers via DNA methylation-dependent repression of SOX9/DEFA5 and DNA methylation-independent induction of OSR1/RIP140 in Caco-2 cells, which may be relevant to crypt-associated epithelial function and gastrointestinal safety.

Identifying effective molecular targets for treatment and enhancing sensitivity to gemcitabine (GEM) could significantly improve the management of PDAC patients...SUZ12 expression is found to be elevated in GEM-resistant (GR) PDAC cells, and decrease of SUZ12 levels increases GEM sensitivity in PDAC cells. The combination of SUZ12 knockout with GEM shows enhanced synergistic effects in cancer therapy and sensitizes GR cells to GEM, providing new insights into overcoming GEM resistance and highlighting SUZ12 as a potential target for clinical intervention in PDAC patients.

Collectively, these findings suggest that honey may safeguard skin stem cells from UV-induced aging by modulating pluripotency and senescence-associated genes and regulating differentiation through alterations in Wnt signaling. Furthermore, Hsp70 upregulation in fibroblasts appears to strengthen cellular stress responses and support homeostatic stability.

Lactate induces YBX1 nuclear translocation, which in turn activates LDHB transcription. Collectively, our findings demonstrate the oncogenic roles of YBX1 and LDHB in ICC progression, identify lactate as a key energy source sustaining the activity of TCA cycle and oxidative phosphorylation, and highlight the YBX1-LDHB axis as a potential therapeutic target.

Future research must prioritise multi-targeted approaches, integrate CSC endpoints into clinical trials and develop predictive biomarkers of CSC burden. Addressing CSC-mediated relapse is essential for advancing precision oncology and achieving lasting therapeutic responses.

Mechanistically, NEK6 bound to Y-box binding protein-1 (YBX1) in the cytoplasm and facilitated its phosphorylation at serine 102 (p-YBX1S102), which promoted YBX1 nuclear translocation and further activated CDK2 and bcl2 transcription. As such, these data provided robust pre-clinical mechanistic evidence of synergy between NEK6 and CDK4/6 inhibitors and delineated a path for translation of these findings to preliminary clinical studies in EC patients.

SRY-box transcription factor 9 was highly expressed in GBM and this activated CLCF1 expression as one of its transcription factors to further enhance GBM development. Thus, CLCF1 regulated by SOX9 can enhance the development and immune evasion of GBM.