<p>Lnc-CHAF1B-2, a newly discovered long noncoding RNA (lncRNA), plays a significant role in the evolution and prognosis of diverse neoplasms. However, its role in the development of gastric cancer is not yet fully understood. Using bioinformatics analysis of gastric cancer RNA-seq data from The Cancer Genome Atlas (TCGA) database, we investigated the expression of lnc-CHAF1B-2 in gastric carcinoma and its associated molecular signalling pathways. Verification through an array of in vivo and in vitro experiments—namely, EdU incorporation, flow cytometry, trans-well migration and invasion assays, subcutaneous tumour formation in nude mice, and western blot analysis—was conducted. We revealed notable upregulation of lnc-CHAF1B-2 in gastric cancer tissues. Furthermore, a positive correlation was detected between lnc-CHAF1B-2 levels and the occurrence of distant metastases in patients, which was inversely related to their prognostic outlook and survival rates. Moreover, our findings confirmed that lnc-CHAF1B-2 enhanced the proliferation, invasion, and migration of gastric cancer cells while inhibiting apoptosis both in vitro and in vivo. Mechanistically, lnc-CHAF1B-2 promoted the progression of gastric cancer through activating the Wnt/β-catenin signalling pathway. Thus, lnc-CHAF1B-2 and its regulation of the Wnt/β-catenin signalling pathway have emerged as prospective therapeutic targets in gastric cancer management.</p>

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lncRNA CHAF1B-2 contributes to the tumorigenesis of gastric cancer by activating the Wnt/β-catenin pathway

  • Shao-Qi Tian,
  • Jun-Jie Shen,
  • Dao-Ping Sun,
  • Wen-Ming Chen

摘要

Lnc-CHAF1B-2, a newly discovered long noncoding RNA (lncRNA), plays a significant role in the evolution and prognosis of diverse neoplasms. However, its role in the development of gastric cancer is not yet fully understood. Using bioinformatics analysis of gastric cancer RNA-seq data from The Cancer Genome Atlas (TCGA) database, we investigated the expression of lnc-CHAF1B-2 in gastric carcinoma and its associated molecular signalling pathways. Verification through an array of in vivo and in vitro experiments—namely, EdU incorporation, flow cytometry, trans-well migration and invasion assays, subcutaneous tumour formation in nude mice, and western blot analysis—was conducted. We revealed notable upregulation of lnc-CHAF1B-2 in gastric cancer tissues. Furthermore, a positive correlation was detected between lnc-CHAF1B-2 levels and the occurrence of distant metastases in patients, which was inversely related to their prognostic outlook and survival rates. Moreover, our findings confirmed that lnc-CHAF1B-2 enhanced the proliferation, invasion, and migration of gastric cancer cells while inhibiting apoptosis both in vitro and in vivo. Mechanistically, lnc-CHAF1B-2 promoted the progression of gastric cancer through activating the Wnt/β-catenin signalling pathway. Thus, lnc-CHAF1B-2 and its regulation of the Wnt/β-catenin signalling pathway have emerged as prospective therapeutic targets in gastric cancer management.