Bioinformatics methods were used to analyze the role of PCAT6 in a variety of tumors and verify its role in oesophageal squamous cell carcinoma (ESCC) EC109 cells. The pan-cancer dataset was downloaded from the University of California Santa Cruz (UCSC) database to analyze the expression of PCAT6 in pan-cancer and its relationship with prognosis, clinical features, and immune infiltration. The expression and prognosis of PCAT6 in ESCC were verified by Gene Expression Omnibus (GEO) and Kaplan-Meier database. CCK8, colony formation, wound healing, Transwell cell invasion (CI), and cell migration (CM) assays were used to detect the effect of PCAT6 knockdown on the ability of ESCC cell proliferation (CP), CI and CM. Gene Set Enrichment Analysis was used to analyze the signaling pathways involved in the regulation of PCAT6. Quantitative real-time PCR and western blotting were used to examine the expression of cancer stem cell-related markers and the activation of JAK/STAT pathway in ESCC after PCAT6 knockdown. PCAT6 is significantly up-regulated in a variety of tumor tissues, and its expression is closely related to prognosis, clinical features and immune infiltration. High expression of PCAT6 leads to poor prognosis in ESCC patients. In ESCC EC109 cells, PCAT6 knockdown inhibited the ability of CP, CI, CM, and stemness, and inhibited the activation of JAK/STAT signaling pathway. PCAT6 expression is elevated in a variety of tumors. PCAT6 plays an oncogene role in ESCC by activating the JAK/STAT signaling pathway.
Keywords: JAK/STAT pathway; Oesophageal squamous cell carcinoma; PCAT6; Pan-cancer; lncRNA.
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