Key result
Alteration of Ftx expression induced significant proteomic changes in highly metastatic HCT116 cells, identifying 556 upregulated and 367 downregulated proteins in Ftx-silenced cells.
Why the study?
The long noncoding RNA Ftx is involved in distant metastasis in colorectal cancer, but Ftx alteration-induced proteomic changes in highly metastatic cells were not investigated.
Alteration of Ftx expression induces proteomic changes in highly metastatic HCT116 cells, suggesting its potential as a biomarker and therapeutic target for metastatic colorectal cancer.
Cell-based Ftx proteomic changes should not alter practice; hypothesis-generating for its biomarker role in metastatic colorectal cancer.
BACKGROUND: The long noncoding RNA (lncRNA) five prime to Xist (Ftx) is involved in distant metastasis in colorectal cancer (CRC). This study aimed to investigate Ftx alteration-induced proteomic changes in the highly metastatic CRC cell line HCT116. METHODS: Tandem mass tag (TMT)-based proteomics analysis was performed to detect the differential protein expression in Ftx-overexpressing and Ftx-silenced HCT116 cells. The differentially expressed proteins were classified and characterized by bioinformatics analyses, including gene ontology (GO) annotation, GO/Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway/protein domain enrichment analyses, as well as hierarchical clustering. A total of 5471 proteins were quantified, and the proteins with |fold change|≥ 1.2 and p < 0.05 were identified as differentially expressed proteins in response to Ftx overexpression or silencing. RESULTS: The bioinformatics analyses revealed that the differentially expressed proteins were involved in a wide range of GO terms and KEGG signaling pathways and contained multiple protein domains. These terms, pathways, and protein domains were associated with tumorigenesis and metastasis in CRC. CONCLUSIONS: Our results indicate that the alteration of Ftx expression induces proteomic changes in highly metastatic HCT116 cells, suggesting that Ftx and its downstream molecules and signaling pathways could be potential diagnostic biomarkers and therapeutic targets for metastatic CRC.
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Jia et al. (2022) studied Colorectal cancer. Ftx overexpression or silencing vs. Mock control (empty vector or scrambled shRNA) was evaluated on Differentially expressed proteins (p=<0.05). Alteration of Ftx expression induced significant proteomic changes in highly metastatic HCT116 cells, identifying 556 upregulated and 367 downregulated proteins in Ftx-silenced cells.
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