EIF3C (Eukaryotic Translation Initiation Factor 3 Subunit C)

In addition, 135 paraffin-embedded serous ovarian cancer samples and 36 paratumor samples were assessed for eukaryotic translation initiation factor 3 subunit C-like protein expression using immunohistochemistry.ResultsBoth protein and messenger RNA expression levels of eukaryotic translation initiation factor 3 subunit C-like were higher in serous ovarian cancer samples than in paratumor samples, and its high expression was associated with poor overall survival in patients with serous ovarian cancer. In addition, multivariate Cox regression analysis showed that high expression of eukaryotic translation initiation factor 3 subunit C-like was an independent poor prognostic factor for patients with serous ovarian cancer.ConclusionsEukaryotic translation initiation factor 3 subunit C-like is upregulated in serous ovarian cancer samples, and it may be recommended as a useful poor prognostic biomarker in patients with serous ovarian cancer.

Through gene ontology enrichment analysis, we identify known pathways involved in melanoma, actinic keratoses, and squamous cell carcinoma and uncover additional pathways. We also uncover 5 protein-coding variants, which, to our knowledge, have not been previously reported, including LRP3 for lipomas, PLCD1 for sebaceous cysts, EIF3CL for lichen planus, TTK for pilonidal cysts, and MAPK15 for systemic lupus erythematosus.

Our results unequivocally demonstrate the anti-tumor efficacy of high salt against breast cancer cells, suggesting its potential as a therapeutic strategy in cancer treatment.

Melanoma was among the top ten diseases associated with the corresponding (106) miRNAs. Our results shed light on melanoma pathogenesis and biologically significant molecular interactions.

There is a correlation between overexpression of EIF3C in tumour tissues of ovarian cancer patients and this is associated with a poorer prognosis. By influencing the p53 signaling pathway, EIF3C facilitates the growth and infiltration of cells in ovarian cancer.

Our findings suggest that EIF3C plays a significant role in NPC progression and immune modulation, particularly in CD8+ T-cell infiltration. Furthermore, the ETS model holds promise as both a prognostic predictor for NPC patients and a tool for adjusting individualized immunotherapy strategies.

In comparison to monotherapy utilizing the chemotherapeutic agent cisplatin, Iacs-eif3c-RNA exhibited superior anti-tumor efficacy and favorable biosafety. The utilization of Iacs-eif3c-RNA as a carrier-free nanotherapeutic agent presents a promising and innovative approach for addressing HNC treating challenges. Moreover, this strategy demonstrates potential for the translation of therapeutic siRNAs into clinical drugs, extending its applicability to the treatment of other cancers and various diseases.

After validation by RT-qPCR and western blot, three downstream genes (APP, HSPA1A, and LMNB1) were confirmed. EIF3C overexpression may facilitate the proliferation and hamper the apoptosis of lung cancer cells by regulating the APP/HSPA1A/LMNB1 axis.

In this study, the Lentivirus-mediated EIF3C shRNA vector (L.V-shEIF3C) was constructed to down-regulate the expression of EIF3C in human pharyngeal squamous carcinoma cell FaDu and the human nasopharyngeal carcinoma cell 5-8F, it was found that down-regulation of EIF3C could significantly inhibit the cell proliferation, promote cell apoptosis, induce cell cycle arrest, and inhibit the formation and growth of tumors in mouse models. This study provides strong evidence that EIF3C is a key gene driving the development and progression of head and neck cancer, which is of great significance for the diagnosis, prognosis or treatment of tumors, suggesting that EIF3C may become a valuable therapeutic development and intervention target.

Our findings demonstrate that FOXO4-mediated upregulation of circPDE5A controls PCa metastasis via the circPDE5A-WTAP-EIF3C-MAPK signaling pathway and could serve as a potential therapeutic targer for PCa.

We validated the observed changes in gene/protein expression in vitro and confirmed our cell line-based studies in the bone marrow of an AML PDX model after Ven-PegC treatment. These results support examining alterations in the translatome post-chemotherapy to offer insight into drug mechanism of action and to inform future therapeutic decisions.