MYC inducible lncRNA inactivating p53 (MILIP)

MYC inducible lncRNA inactivating p53 (MILIP), also known as MAFG-AS1 and related synonyms, is a long non-coding RNA upregulated by oncogenic signals such as MYC and plays a regulatory role by functioning as a competing endogenous RNA (ceRNA). MILIP is found primarily in the cytoplasm, where it absorbs various tumor-suppressive microRNAs, thereby facilitating the expression of protein-coding oncogenes. This lncRNA drives cancer cell proliferation, suppresses apoptosis, promotes migration, invasion, epithelial-to-mesenchymal transition, glycolysis, and contributes to tumor drug resistance, with significant involvement in the progression of multiple cancers (including hepatocellular carcinoma, breast, bladder, and esophageal cancers)[1][2][3][4][6]. High MILIP/MAFG-AS1 expression has been correlated with poor prognosis and resistance to targeted therapies. It is under investigation both as a biomarker for cancer prognosis and drug response, and as a novel therapeutic target in cancer biology[1][2][3][5].

Other names

MAFG-AS1MAFG-DTMAFG antisense RNA 1 (head to head)MAFG antisense RNA 1 (non-protein coding)MAFG divergent transcriptc-Myc-Inducible Long noncoding RNA Inactivating P53

Targeting MILIP/MAFG-AS1 can decrease cancer cell proliferation, migration, invasion, induce apoptosis, and reverse drug resistance by modulating downstream axis (e.g., miR-3196/STRN4, miR-143-3p/SERPINE1, miR-765/PDX1) and signaling pathways (e.g., JAK2/STAT3). MILIP acts as a ceRNA, sponging tumor-suppressive miRNAs and facilitating oncogene expression[1][2][3][4][6]