ACTG1 (Actin Gamma 1)

Critically, overexpression of COL21A1 rescued the inhibitory effects of ACTG1 knockdown on proliferation, migration, and EMT. These findings demonstrate that the ACTG1/COL21A1 axis promotes GC progression by regulating EMT, highlighting its potential as a therapeutic target for patients with GC.

In addition to detailing specific features of our case, we also discuss those differences that may help distinguish ACTG1::MITF fusions from other clear cell tumors. Considering the significant differences in clinical outcomes between these distinct classes of clear cell tumors, accurate distinction can significantly affect management options.

Collectively, our findings demonstrate that OTUD6A promotes dopaminergic neuron degeneration and PD progression by deubiquitinating and stabilizing ACTG1, which in turn activates a p53-dependent apoptotic pathway. These findings identify OTUD6A as a potential therapeutic target for PD intervention.

Based on human HCC data, SPP1, NQO1, RRM2, APOA1, APOC3, ALDOB, and IGF1 were identified as prognosticators indicating poor overall survival. This study presents the first cross-species transcriptomic analysis of canine HCC, revealing significant molecular resemblances to human HCC, indicating it may be a promising comparative model for studying tumor biology, drug responses, and novel therapeutic interventions.

This study reveals that a B cell subpopulation characterized by the co-expression of HLA-DRB5, HLA-DQA2, HLA-DQB1, CD74, and ACTG1 is significantly associated with nCRT response in rectal cancer. These findings offer actionable insights for optimizing clinical treatment strategies, including patient stratification and personalized therapy selection.

Histopathological examination confirmed a GLI1-altered mesenchymal tumor, and RNA sequencing identified a novel ACTG1::GLI1 fusion, representing the first documented case of ACTG1 as a fusion partner for GLI1. By reviewing the literature, we further characterize the morphologic, immunophenotypic, and molecular genetic spectrum of this rare ovarian neoplasm, expanding the known diversity of GLI1-associated fusions in mesenchymal tumors.

Target prediction and functional annotation identified 59 overlapping genes, with the Proteoglycans in cancer pathways being conserved in both species, mediated by ACTG1, SDC1, FRS2, and WNT9B. Collectively, these findings demonstrate distinct intra-tumoral and exosomal expression pattern of miR-10a in canine HCC and support its potential as a non-invasive biomarker with translational relevance.

Furthermore, the ferroptosis inducer RSL3 synergized with cisplatin to enhance ferroptosis and mitochondrial fragmentation, effectively sensitizing ACTG1-overexpressing cells both in vitro and in xenograft models. Our findings establish ACTG1 as a critical mediator of cisplatin resistance in NSCLC through regulation of mitochondrial integrity and ferroptosis. Targeting the ACTG1-MFN2 axis combined with ferroptosis induction represents a promising therapeutic strategy to overcome cisplatin resistance.

These findings highlight the pivotal role of ACTG1 in regulating EMT in BLCA through its splicing activity on P4HB, suggesting new therapeutic targets for intervention. This study underscores the critical importance of splicing regulation in cancer biology, offering novel insights for diagnostic and therapeutic strategies in BLCA.

Our data reveal novel insights into the role of amisulpride in modulating the differential expression of genes and proteins. These findings, which involve genes/proteins related to AP-1 transcription factor family gene regulation, cytoskeleton, histone binding activity, the intracellular trafficking of receptors and endocytosis of a variety of macromolecules, and nuclear localization signal, are particularly significant as they shed light on the molecular underpinnings of the clinical efficacy of amisulpride and the pathogenesis of schizophrenia.

These findings demonstrate that surface biotinylation improves the sensitivity and selectivity of plasma membrane proteomics under hypoxia, revealing hypoxia-responsive proteins and pathways not captured by standard whole-cell analysis.