TRIM21 (Tripartite Motif Containing 21)

This research, we identified that RAB40C, an oncogene, was a target of STAT3 and boosted the malignant progression of HCC by regulation of EGFR cascades, and exerted a promising potential in HCC therapy.

This review systematically summarizes recent breakthroughs in controllable TPD strategies, elucidates their distinct molecular mechanisms, and highlights their promising therapeutic applications. The rapidly evolving field of controllable TPD represents a powerful and adaptable technological frontier, opening new avenues in precision medicine and providing versatile tools for the future of biomedical research.

Moreover, the concomitant upregulation of TAF1 and KCTD9 Kbhb serves as a poor prognostic factor for metastatic CRC patients. Taken together, our findings bridge the newly identified Kbhb modification dependent regulatory mechanism that modulates the anticancer function of KCTD9, and provided insight into potential strategies for targeting epigenetic factor and combating the KCTD9 inactive-driven CRC metastasis.

TRIM21/CERKL/autophagy pathway exists in PC.

While the cells were treated with chloroquine (CQ), an autophagy inhibitor, the expression of Cl...Mechanistically, TRIM21 loss inhibited the AKT/mTOR signaling pathway, thereby regulating cell growth and inducing autophagy-mediated apoptosis. Collectively, our findings provide novel insights into the role of TRIM21 in ESCC and offer a potential therapeutic target for ESCC.

This innovative light-inducible protein degradation system offers a powerful approach to investigate the functions of specific proteins within physiological contexts. Moreover, Flash-Away presents potential opportunities for clinical translational research and precise medical interventions, advancing the prospects of precision medicine.

This study reveals a novel function of SNAP23, independent of vesicle transport, mediating crosstalk between the cell membrane and mitochondria to influence the chemotherapeutic response to oxaliplatin (OXA)...This reduces the ubiquitination and degradation of the mitochondrial transcription factor A (TFAM), enhancing mitochondrial oxidative metabolism and increasing oxidative phosphorylation (OXPHOS) and reactive oxygen species (ROS) production, ultimately heightening the sensitivity of cancer cells to OXA. The unique regulatory function of SNAP23 in the chemotherapeutic response of colorectal cancer may provide a potential target for chemotherapy sensitization.

Collectively, our findings establish TREM2+ TAMs as key drivers of GC progression and immune evasion. Targeting TREM2+ TAMs represents a promising therapeutic strategy to overcome resistance to anti-PD-L1 therapy and reshape the tumor immune microenvironment.

These findings indicate that, beyond the canonical GPX4 pathway, the xCT/CD98 complex can inhibit ferroptosis via the TRIM21/RACK1/FPN1 axis. Targeting RACK1 offers a potential therapeutic strategy to sensitize tumors to ferroptosis and overcome therapy resistance across multiple cancer types and in people with cancer.

Additionally, the combination of STL127705, an inhibitor of the XRCC6/XRCC5 heterodimer, with radiotherapy notably suppressed tumor growth in patient-derived xenograft (PDX) and cell line mouse transplant tumor models, especially in the context of CNOT7 deficiency. These findings elucidate the function of CNOT7 in promoting DNA repair and radiotherapy resistance in CRC, highlighting that targeting the CNOT7-TRIM21-XRCC6 axis provides a promising therapeutic approach to overcome radiotherapy resistance and improve clinical outcomes for CRC patients.

Clinically, high USP18 levels are associated with worse patient prognosis. Our findings underscore the critical role of USP18 in modulating DDR signaling and radiosensitivity in NPC, suggesting that targeting the USP18-TRIM21-TRIM29 axis may represent a novel strategy to enhance the efficacy of radiotherapy for patients with NPC.

These findings reveal that FAM135B regulates the IFI16-dependent STING pathway and subsequent immune activation. FAM135B may represent a potential predictor of ICB therapeutic responses for TNBC patients.