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 This evidence concerns the gene LINC00511 and breast carcinoma.