Epigenetically induced MYC interacting lncRNA 1 (EPIC1)

Epigenetically induced MYC interacting lncRNA 1 (EPIC1, also known as Lnc-EPIC1) is a long non-coding RNA predominantly localized to the nucleus[1]. It is subject to epigenetic regulation (notably, promoter region methylation/hypomethylation)[1]. In cancer, EPIC1 is frequently overexpressed, correlating with poor clinical outcome in subtypes like luminal B breast cancer[1]. EPIC1 exerts its function by directly binding the MYC protein via a defined sequence motif (129–283 nucleotides of EPIC1) to the 148–220 amino acid region of MYC, enhancing MYC’s transcriptional activities, promoting cell cycle progression, tumor cell proliferation, and anchorage-independent growth in vitro and in vivo[1][2][4].\n\nBeyond its cancer-proliferative role, EPIC1 participates in resistance mechanisms: high EPIC1 levels upregulate the AKT-mTORC1 signaling pathway, leading to resistance against mTOR inhibition (such as rapamycin) in breast and ovarian cancer cell lines[2]. EPIC1 is also crucial for cell survival in neural tissues, mitigating oxidative stress-induced neuronal death by supporting MYC-dependent transcription of survival genes; downregulation of EPIC1 exacerbates cell death under stress conditions[4].\n\nGene silencing approaches (e.g., siRNA/shRNA) against EPIC1 suppress cell proliferation, induce cell cycle arrest, and reduce tumorigenesis, indicating its potential as a therapeutic target, particularly for MYC-driven or rapamycin-resistant cancers[1][2].\n\nThere are currently no clinically approved drugs or small molecules known to directly target EPIC1; research is ongoing in understanding its regulation and therapeutic potential.

Other names

Lnc-EPIC1epigenetically-induced lncRNA1EPIC1

Drugs indirectly affecting EPIC1 function (e.g., targeting the mTORC1 pathway with rapamycin).\nGene silencing (siRNA/shRNA targeting EPIC1) reduces proliferation and tumor growth[1][2].