LINC00511 and colorectal cancer: For example, in breast cancer, LINC00511 was shown to foster progression by competitively binding miR‐150 with MMP1323; in colorectal cancer, LINC00511 acted as a carcinogen by suppressing IL‐24 expression through interaction with EZH224; additionally, LINC00511 facilitated carcinogenesis by recruiting EZH2 to the PTEN promoter, enhancing methylation of the PTEN promoter, and activating downstream signaling pathways influencing gastric cancer proliferation.25