In recent years, increasing evidence has shown the potential role of long non-coding RNAs (lncRNAs) in multiple cancers. Deregulation of lncRNAs was detected being closely associated with many kinds of tumours where they can act as a tumour suppressor or accelerator. LINC00152 was identified as an oncogene involved in many kinds of cancers, such as gastric cancer, hepatocellular carcinoma, colon cancer, gallbladder cancer and renal cell carcinoma. Moreover, inhibition of LINC00152 can suppress proliferation, migration and invasion of the cancer cells. Increasing evidence has showed that LINC00152 may act as a diagnostic and prognostic biomarker for the above-mentioned cancers.
Underlying regulatory mechanisms of LINC00152 in human cancers
(A) LINC00152 may interact with THBS1 mediated by miR-18a-5p. (B) LINC00152 may act as a competing endogenous RNA (ceRNA) to regulate the expression of miR-193a-3p, and then regulate ERBB4. (C) LINC00152 can activate the mechanistic target of rapamycin (mTOR) pathway by binding to the promoter of EpCAM. (D) LINC00152, which can be activated by SP1, can participate in the phosphatidylinositol 3-kinase (PI3K)/AKT signalling pathway. (E) LINC00152 can facilitate GC cell proliferation by accelerating the cell cycle by binding to enhancer of zeste homologue 2 (EZH2) and silencing the expression of p15 and p21. (F) LINC00152 can promote the epithelial to mesenchymal transition (EMT) programme