FSCN1 (Fascin Actin-Bundling Protein 1)

Unlike conventional markers that often reflect tumor-specific traits, this panel captures the mechanical and structural determinants of cell invasiveness. The robustness of these genes across diverse molecular assays and their alignment with core metastatic pathways underscore their translational relevance.

Furthermore, concerns were raised regarding Figures 2c, 2e, 4f and 5 g, where the western blot backgrounds appear unusually clean, deviating from typical experimental results. Due to the nature of these concerns and the absence of author response, the journal has decided to issue an Expression of Concern to inform and alert readers.

Although temozolomide (TMZ) is a cornerstone of GBM treatment, its efficacy is often compromised by inherent or acquired resistance, underscoring the urgent need to uncover molecular mechanisms, discover new therapeutic targets, and develop innovative treatment strategies. Importantly, combining the FSCN1 inhibitor NP-G2-044, with TMZ therapy resulted in stronger anti-tumor effects both in vitro and in vivo. In conclusion, the study demonstrates that nuclear F-actin formation in GBM promotes DSB repair and reveals that targeting FSCN1 with NP-G2-044 could be a promising strategy for enhancing treatment outcomes and improving the prognosis for GBM patients.

Our findings reveal a novel RNA-binding function of FSCN1 in posttranscriptional regulation of THBS1, establishing the FSCN1/THBS1/TGF-β axis as a critical driver of ESCC progression. The acetylation-dependent modulation of this pathway highlights the potential therapeutic vulnerability of metastatic ESCC cells.

In summary, our research established the ARG-derived prognostic signature validated across independent GBM cohorts and revealed concomitant immune and mechanical niche dysregulation in high-risk patients. The rationale for combined angiogenesis/stroma/immune modulation strategies was provided, with FSCN1 proposed as the potential therapeutic target.

Immunohistochemistry in samples from 68 patients demonstrated significant correlations between fascin and Ki-67 expression, in addition to SKP2 overexpression and p27 downregulation. Collectively, these data demonstrate the role of fascin as a driver of the G1-S-phase transition during cell cycle proliferation, thereby revealing new opportunities for targeted therapeutic intervention.

This study provides a comprehensive exploration of the metabolic characteristics of malignant cells in lung cancer at single-cell resolution. Our findings provide insights that could improve prognosis and support more targeted treatments for lung cancer patients.

These findings highlight the dual role of fascin in tumor cells and the tumor microenvironment (TME), and reinforce its potential as a biomarker for personalized TNBC therapies. Ongoing clinical trials, including HITCLIF, are exploring the efficacy of imipramine in patients with fascin-overexpressing cancers, paving the way for targeted treatment strategies.

The data obtained demonstrated the feasibility of using these ABPs as additional predictors of  NSCLC prognosis.

Furthermore, this review highlights emerging therapeutic opportunities, including targeting FSCN1 (Fascin Actin-bundling Protein 1, FSCN1) inhibition or using small-molecule inhibitors to disrupt oncovirus-mediated cytoskeletal changes and impede tumor progression. By bridging virology and cancer biology, this review provides novel insights for developing precision antimetastatic strategies and underscores the pivotal role of viral-cytoskeletal interplay in oncology.

The expression of FRA1 and its target genes correlates with shortened survival across multiple cancer types, highlighting the broader clinical relevance of this pathway. This study unveils an actionable FRA1-mediated transcriptional network that drives cancer progression and metastasis, offering potential avenues for therapeutic interventions.

The phenotypic characteristics of the CAR-T cells, including memory T cell subsets (stem cell memory and central memory), were analyzed by flow cytometry. Tumor growth inhibition was assessed, and markers of immune exhaustion and evasion were quantified.