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. 2015 Feb 18;9:1103–1175. doi: 10.2147/DDDT.S73551

Figure 12.

Figure 12

Proposed mechanisms for how hsa-miR-181a regulates cancer genes and may serve as an oncogene for the development of EC.

Notes: hsa-miR-181a may play a role in the tumorigenesis of EC via multiple pathways that interplay with many important oncogenes and tumor suppressors. hsa-miR-181a may interact with H3F3B, ATM, CCDC6, TAF15, RAS, and PLAG1 to promote cell proliferation. It may suppress cell apoptosis via interaction with NOTCH1, NOTCH2, MAPK1, and BCL2. It may affect ubiquitin-mediated proteolysis via regulation of FBXO11, STAG2, BRCA2, HOXA11, and RBM15. All these actions may transform the normal endometrial cells into tumor cells.

Abbreviation: EC, endometrial cancer; ATM, ATM serine/threonine kinase; BCL2, B-cell lymphoma 2; CCDC6, coiled-coil domain containing 6; PLAG1, pleiomorphic adenoma gene 1; MAPK1, mitogen activated kinase-like protein 1; RAS, rat sarcoma viral oncogene homolog; BRCA2, breast cancer 2, early onset; STAG2, stromal antigen 2; HOXA11, homeobox A11; RBM15, RNA binding motif protein 15; NOTCH1, notch 1; H3F3B, H3 histone, family 3B; FBXO11, F-box protein 11; TAF15, TAF15 RNA polymerase II, TATA box binding protein (TBP)-associated factor, 68 kDa; HOOK3, hook microtubule-tethering protein 3; PTPN11, protein tyrosine phosphatase, non-receptor type 11; TSHR, thyroid stimulating hormone receptor; CDX2, caudal type homeobox 2; EP300, E1A binding protein p300.