FSCN1 (Fascin Actin-Bundling Protein 1)

Overall, our study indicates that the molecular mechanisms underlying disturbed PNP in IPMNs are not mediated by a single pathway but involve multiple interconnected pathways. Our findings may contribute to elucidation of the molecular mechanisms regulating PNP in IPMNs, enhancing our understanding of tumor progression and contributing to more accurate pathological diagnosis.

Proteomic profiling revealed that TDECs shift from an adhesion-anchored to a microtubule-rich and glycolytically rewired phenotype, with upregulation of vesicle-trafficking regulators (ARF1/3/4, ANXA2/5), migration drivers (RAC1/3, RHOA/C, WDR1, FSCN1) and glycolytic enzymes (ENO1, ALDOA, PKM, LDHA), alongside the suppression of integrin- and cytoskeletal-anchoring proteins. Collectively, these findings indicate that tumor-ECM-driven endothelial apoptosis generates reversible reprogramming and an EV-mediated autocrine mechanism that may favor angiogenic balance.

5 prognosis-relevant LRGs could provide a novel perspective for the individualized therapeutic regimens for LUAD.

PDE3A plays a pivotal role in tumorigenesis and cancer progression, with aberrant expression strongly associated with tumor proliferation, metastasis, and resistance to chemotherapy. As a therapeutic target, PDE3A holds significant potential. The development of PDE3A inhibitors or molecular adhesive agents may offer novel treatment strategies, particularly for chemotherapy-resistant tumor types.

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.