LCP1 (Lymphocyte cytosolic protein 1)

Further research revealed that LINC02613 interacts with lymphocyte cytosolic protein 1 (LCP1), shielding its ubiquitination site and interfering with its normal ubiquitination degradation process, thereby promoting OSCC metastasis and progression. Using pH-responsive nanoparticles (PLGA-Dlink) loaded with siLINC02613 for targeted delivery in vivo and in vitro, we successfully inhibited OSCC metastasis and progression, providing a new potential therapeutic approach for OSCC treatment.

Functional assays revealed that LCP1 expression promoted tumor growth in vivo and enhances proliferation, migration, invasion, and cisplatin resistance in vitro across four OSCC cell lines...Additionally, LCP1 activated the JAK2/STAT3 axis to upregulate pro-interleukin-1β (IL-1β) expression and IL-1β secretion, thereby amplifying OSCC cell aggressiveness. In summary, this study provides novel insights into the oncogenic role of LCP1 in OSCC, linking EGFR-mediated signals and IL-1β production, and identifies LCP1 as a promising target for therapeutic intervention.

Therefore, like other cytoskeleton pH sensors, plastins promote disassembly and faster dynamics of cytoskeletal components during cytokinesis and cell migration. Since both plastins are implemented in cancer, their pH sensitivity may contribute to the accelerated proliferation and enhanced invasive and metastatic potentials of cancer cells at alkaline pHi.

Therefore, like other cytoskeleton pH sensors, plastins promote disassembly and faster dynamics of cytoskeletal components during cytokinesis and cell migration. Since both plastins are implemented in cancer, their pH sensitivity may contribute to the accelerated proliferation and enhanced invasive and metastatic potentials of cancer cells at alkaline pH i .

The Gene Ontology and pathway analyses highlighted that several proteins (e.g., small integral membrane protein 22, cofilin-1, macrophage-capping protein, plastin-2, and biliverdin reductase A) were linked to innate immune responses and actin cytoskeleton remodeling, which is a critical event in liver fibrosis and cancer progression. These findings provide new foundations for a deeper understanding of the pathophysiology of PSC and demonstrate that saliva is a suitable biological sample for obtaining proteomic fingerprints useful in the search for biomarkers capable of discriminating between the two cholestatic diseases.

LCP1 could be a potential therapeutic target for patients with OC who are resistant to olaparib. Our study provides a new mechanism of olaparib resistance.

LCP1 may serve as a potential diagnostic and prognostic biomarker for TNBC, which was closely associated with immune cell infiltration, particularly M1 and M2 macrophages. Our findings may provide valuable insights into immunotherapeutic strategies for TNBC patients.

This study identified 9 immune cell-related biomarkers that may be actively involved in the progression of EGC and serve as potential targets for GC diagnosis and treatment.

Our work showed that the analysis of FFPE samples was able to identify key proteins that might be crucial for the IPF pathogenesis. These proteins are correlated with lung carcinogenesis or involved in the immune landscape of lung cancer, thus making possible common mechanisms between lung carcinogenesis and fibrosis progression, two pathological conditions at risk for each other in the real life.

The ability to isolate functional NK-EVs on a large scale and use them with platinum-based drugs may lead to new clinical applications. The results of the present study suggest the possibility of the combination of NK-cell-derived EVs and CBP as a viable immunochemotherapeutic strategy for resistant cancers.

Furthermore, immunomodulatory factors involved in immune infiltration and migration including interleukin-8, lymphocyte cytosolic protein 1, and transgelin-2, were upregulated upon inhibition of ERO1a and IDO1. Collectively, our results show that inhibition of ERO1a and IDO1 modulates the tumor microenvironment associated with improved monocyte infiltration and differentiation into dendritic cells to potentially influence therapeutic responses in patients with PDAC.