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Inhibiting the expression of spindle appendix cooled coil protein 1 (SPDL1) can slow down disease progression and is related to poor prognosis in patients with esophageal cancer. However, the specific roles and molecular mechanisms of SPDL1 in esophageal squamous cell carcinoma (ESCC) have not been explored yet. The current study aimed to investigate the expression levels of SPDL1 in ESCC via transcriptome analysis using data from The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus databases. Moreover, the biological roles, molecular mechanisms, and protein networks involved in SPDL1 were identified using machine learning and bioinformatics. The cell counting kit-8 assay, EdU staining, and transwell assay were used to investigate the effects of inhibiting SPDL1 expression on ESCC cell proliferation, migration, and invasion. Finally, the correlation between the SPDL1 expression and cancer immune infiltrating cells was evaluated by analyzing data from the TCGA database. Results showed that SPDL1 was overexpressed in the ESCC tissues. The SPDL1 expression was related to age in patients with ESCC. The SPDL1 co-expressed genes included those involved in cell division, cell cycle, DNA repair and replication, cell aging, and other processes. The high-risk scores of SPDL1-related long non-coding RNAs were significantly correlated with overall survival and cancer progression in patients with ESCC (P < 0.05). Inhibiting the SPDL1 expression was effective in suppressing the proliferation, migration, and invasion of ESCC TE-1 cells (P < 0.05). The overexpression of SPDL1 was positively correlated with the levels of Th2 and T-helper cells, and was negatively correlated with the levels of plasmacytoid dendritic cells and mast cells. In conclusion, SPDL1 was overexpressed in ESCC and was associated with immune cells. Further, inhibiting the SPDL1 expression could effectively slow down cancer cell growth and migration. SPDL1 is a promising biomarker for treating patients with ESCC.
Inhibiting the expression of spindle appendix cooled coil protein 1 (SPDL1) can slow down disease progression and is related to poor prognosis in patients with esophageal cancer. However, the specific roles and molecular mechanisms of SPDL1 in esophageal squamous cell carcinoma (ESCC) have not been explored yet. The current study aimed to investigate the expression levels of SPDL1 in ESCC via transcriptome analysis using data from The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus databases. Moreover, the biological roles, molecular mechanisms, and protein networks involved in SPDL1 were identified using machine learning and bioinformatics. The cell counting kit-8 assay, EdU staining, and transwell assay were used to investigate the effects of inhibiting SPDL1 expression on ESCC cell proliferation, migration, and invasion. Finally, the correlation between the SPDL1 expression and cancer immune infiltrating cells was evaluated by analyzing data from the TCGA database. Results showed that SPDL1 was overexpressed in the ESCC tissues. The SPDL1 expression was related to age in patients with ESCC. The SPDL1 co-expressed genes included those involved in cell division, cell cycle, DNA repair and replication, cell aging, and other processes. The high-risk scores of SPDL1-related long non-coding RNAs were significantly correlated with overall survival and cancer progression in patients with ESCC (P < 0.05). Inhibiting the SPDL1 expression was effective in suppressing the proliferation, migration, and invasion of ESCC TE-1 cells (P < 0.05). The overexpression of SPDL1 was positively correlated with the levels of Th2 and T-helper cells, and was negatively correlated with the levels of plasmacytoid dendritic cells and mast cells. In conclusion, SPDL1 was overexpressed in ESCC and was associated with immune cells. Further, inhibiting the SPDL1 expression could effectively slow down cancer cell growth and migration. SPDL1 is a promising biomarker for treating patients with ESCC.
Background: F-box and leucine-rich repeat protein 18 (FBXL18) is an F-box protein that functions as an E3-ubiquitin ligase, and it plays pivotal roles in multiple disease processes. However, its role and underlying mechanism in ovarian cancer (OC) are still unknown. We investigated the impact and mechanism of FBXL18 in OC cell growth and tumorigenesis. Methods: Silent interfering RNAs and overexpression plasmids were employed to knock down and overexpress FBXL18 in OC cells (A2780 and OVCAR3). CCK-8, colony formation, cell migration, and nude mouse xenograft assays were used to assess the effect of FBXL18 on OC cell proliferation and migration. Western blotting and co-immunoprecipitation followed by ubiquitination assays were performed to detect the mechanism of the FBXL18/AKT axis in OC. Results: FBXL18 knockdown inhibited OC cell proliferation and migration, whereas FBXL18 overexpression showed the opposite results. Phosphorylated-AKT (S473) protein expression was increased by FBXL18 overexpression and markedly decreased after phosphorylated-AKT inhibitor (MK-2206) treatment. Coimmunoprecipitation assays demonstrated that FBXL18 strongly interacted with AKT in OC cells. Ubiquitination assays revealed that FBXL18 promoted K63-linked AKT ubiquitination to activate AKT. MK-2206 treatment reversed the increase in proliferation and migration of OC cells induced by FBXL18 overexpression. Conclusions: FBXL18 promoted OC cell proliferation and migration and facilitated OC tumorigenesis. Mechanically, FBXL18 interacted with AKT and promoted K63-linked ubiquitination of AKT to activate AKT in OC cells. Our study revealed that the FBXL18/AKT axis plays a crucial role in the OC process, indicating that FBXL18 may be a valuable target for OC diagnosis and treatment.
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