YY1-mediated transcriptional regulation of LINC01615 inhibits WNT2 mRNA degradation to promote gastric cancer progression.

Gastric cancer (GC) is a common malignancy of the digestive system, characterized by high invasiveness and metastasis, making it a leading cause of cancer-related deaths. Long non-coding RNAs (lncRNAs) play a crucial role in various types of cancer. This study aimed to elucidate the function of LINC01615 and its potential regulatory mechanisms in GC. In tissue and serum samples from GC patients, LINC01615 expression was significantly elevated and was associated with recurrence, distant metastasis, and TNM stage. LINC01615 promoted the proliferation, migration, and invasion of GC cells, and accelerated the growth of subcutaneous tumors in nude mice. Mechanistically, LINC01615 activated the WNT2/β-Catenin pathway by preventing WNT2 mRNA degradation and enhancing the nuclear translocation of β-Catenin. Furthermore, we identified the transcription factor YY1 as a key regulator of LINC01615 expression, which directly binds to its promoter region. Analysis of clinical samples revealed a positive correlation between the YY1/LINC01615/WNT2 signaling axis and poor prognosis in GC patients. Taken together, this study uncovers that the YY1/LINC01615/WNT2 signaling axis plays a crucial role in GC progression and may serve as a novel diagnostic marker and therapeutic target.